ANALYTICAL  and  DIFFERENTIAL 

DIAGNOSIS  ofNERVOUS  DISEASES 
HENRY  HUN. M.D. 


*v^T 


«*  mf.< 


Columbia  SUntoertfitp 
mtljfCttptjflftoiork 

THE  LIBRARIES 


jftlebical  ilibrarp 


Given  by 

Dr.  Oliver  S.  Strong 


AN  ATLAS 

of  the  m-^w.^sv. 

DIFFERENTIAL  DIAGNOSIS 


OF  THE 


DISEASES  OF  THE  NERVOUS  SYSTEM 


ANALYTICAL    AND    SEMEIOLOGICAL 
NEUROLOGICAL   CHARTS 


BY 

HENRY   HUN.    M.    D. 

FORMERLY  PROFESSOR  OF  Til  I  I  111:   NEKVOCS  SYSTEM  IN  Tilt   AI.HWY    KKMCAX  OOLUBCUS, 

MEMBER    Of   TBI     \MII1H\N    MEDICAL    ASSOCIATION, 

THE    ASSOCIATION    OF    AMERICAN     PHYSICIANS, 
THE    UOnUCAM     Ml  oi.K    \l       Ifli  .oil.vlloN,     FTC, 

AUTHOR  OF   "\    i.cihi:    FOB    \\n  Ki'   >.n    mfihcal  stidfnts   IN    M  10.11:." 
"BTXLABUB  OF   A   001  If   Tin.    skiiviiis  81 


"Ml 
REVISED  AND  ENLARGED 
EDITION 


T««  8oot»wo»tii  I   ■.«!•«■.  i.   I'l IBUSZM1 

TROT,    N*W   YnKK 

1014 


H 
H 


Copyrighted  1912  and  1914  by 
HENRY  HUN,  M.  D. 


*%fr~~f 


To 

Thomas  Hun 

a  loving  father 

a  learned  physician 

a  man  of  wisdom  and  wit 

this  book  is  dedicated 

in  most  grateful  remembrance 


Preface,  Page  1 


CHART 

I. 

II. 

III. 

IV. 

V. 

VI. 

VII. 

VIII. 

IX. 


TABLE  OF  CONTENTS 


PART  ONE 

Semeiology 


Introduction  to  the  Semeiological  Charts 

PAGE 

31. — Case  taking — examination  of  patients;  comprising  numbers  1  to  79. 

49. — Analysis  of  subjective  symptoms;  comprising  numbers  81  to  190. 

53. — Semeiology  of  disordered  mental  activity;  comprising  numbers  200  to  237. 

63. — Semeiology  of  disordered  voluntary  motor  activity;  comprising  numbers  240  to 
293. 

77. — Semeiology  of  disordered  reflex  activity;  comprising  numbers  296  to  341. 

87. — Semeiology  of  disordered  sensory  activity;  comprising  numbers  344  to  392. 

97. — Electrical  examination;  comprising  numbers  395  to  405. 
107. — Examination  of  cerebro-spinal  fluid;  comprising  numbers  410  to  420. 

...  I  Special  syndromes;  comprising  numbers  425  to  458. 

|  Anatomical  terms;  comprising  numbers  460  to  464. 


PART  TWO 

Diagnosis 

Introduction  to  the  Diagnostic  Charts 

X.     125. — Diseases  causing  motor  paralysis  (weakness);  comprising  numbers  469  to  556. 
XI.     133. — Diseases  causing  convulsion  or  spasm;  comprising  numbers  570  to  631. 
XII.     141. — Diseases  causing  perversion  of  motion  (ataxia,  tremor,  nystagmus,  fibrillation), 
also  local  palsies  and  spasms;  comprising  numbers  635  to  7.;.; 

XIII.  155. — Diseases  causing  disorders  of  Speech  ami  gait;  comprising  numbers  736  to  800. 

XIV.  163. — Diseases  causing  diminution  or  exaggeration  of  sensation  (anesthesia,  etc.)  and 

disorders  of  special  senses;  comprising  numbers  804  to  927. 
XV.     175. — Diseases  causing  perversion  of  sensation  (pain  and  vertigo);  comprising  numbers 

930  to  1033. 
XVI.      185. — Diseases  causing  mental  disorders;  comprising  numbers  1036  to  1117. 
XVII.     193. — Diseases  causing  trophic  (change  of  size)  and  sympathetic  (ganglionic  and  vaso- 
motor) disorders;  comprising  numbers  1120  to  1202. 
XVIII.     203. — Diseases  caused  by  syphilis  of  the  nervous  system;  comprising  numbers  1205  to 
1217. 
XIX.     205. — Diseases  associated   with   abnormal  cerebro-spinal   fluid;    comprising    numbers 
1220  to  1242. 

PART   THREE 

Localization 

XX.     209. — Localization  in  spinal  cord;  comprising  numbers  1250  to  1287. 
XXI      217.     Localisation  in  brain;  comprising  numbers  1268  to  1285. 
XXII.     227.    -( iemral  lorali/.itiou  from  symptoms  of  paralysis  or  spasm;  comprising  numbers 
1290  to  1405. 

PLATES 

Erb's  motor  points  for  electrical  examination. 
Erb's  diagram  Bhflffl  mg  the  effects  of  injury  of  a  nerve. 
j  illustrating  laryngeal  paralyses, 

'  ii  ins  of  ocular  paralyses. 
ns  of  the  cerebral  hemispheres. 

I  ulo-motor  nucleus, 

Diagram  of  nuclei  in  brain 

i  ion  through  pons  Varolii. 

ii  the  medulla  oblongata. 

I I  if  the  spinal  cord, 

1 1         f  nuclei  i 

Sobemal  the  more  important  diseases  of  the  spinal  cord. 

Schematic  repi  points  in  the  physiology  and  pathology 

I  diagram  showing  the  motor  and  n  H  of  the  spinal  cord  segments. 

I  diagram  showing  the  cutaneous  distribution  ol  tl  rvesand  nen  e 

Diagram  ol  long  n  d  loi  j  projection 
Diagram  showing  course  ol  gustatorj  fibers. 
I  Hagram  illustrating 

I  showing  llie  nurlei  of  origin  and  the  .1 

sen    0 

INDEX.   Page  387 


FIGCRE 

1  to  5. 

103  3. 

6. 

106. 

7  to  18, 

158. 

14. 

169. 

15  to  17. 

340  1. 

18 

2  12. 

19 

213. 

30 

211 

346. 

2  1  and  26. 

346  7 

2fi 

2  16. 

348 

38  to  31 

340. 

83. 

380. 

381. 

84. 

383. 

86. 

364. 

37. 

384. 

PREFACE 


The  diagnosis  of  diseases  of  the  nervous  system  is  generally  regarded  by 
medical  students  as  one  of  the  most  difficult  subjects  in  their  course  of  study. 
It  is  so  difficult  that  many  students  become  discouraged  and  after  a  few  attempts 
make  no  strong,  continued  effort  to  master  it  and,  perhaps  in  consequence,  physi- 
cians generally  are  weaker  in  this  than  in  other  phases  of  their  work.  In  the 
hope  of  making  this  task  less  difficult  for  both  physicians  and  students  this 
book  has  been  written.  If  the  student  can  be  taught  to  make  the  diagnosis  of 
these  diseases  with  comparative  ease,  it  may  happen  that  he  will  be  led  to  under- 
take those  further  studies  in  the  finer  anatomy  and  physiology  of  the  nervous 
system,  which  are  essential  for  a  full  understanding  of  this  difficult  but  fascinat- 
ing department  of  medicine. 

A  careful  physical  examination  and  history  of  the  case,  as  complete  as  can 
be  obtained,  are,  of  course,  the  essential  basis  of  every  diagnosis;  but  the  com- 
monly employed  method  of  comparing  the  combination  of  symptoms  thus 
obtained  in  any  case  with  the  various  syndromes  characteristic  of  the  different 
diseases  until  a  similar  combination  can  be  found,  is  not  altogether  satisfactory. 
More  scientific  and  instructive  is  the  analysis  of  each  important  symptom  and 
the  consequent  ascertaining  of  the  disease  which  must  cause  it  under  the  cir- 
cumstances (the  other  symptoms)  existing  in  any  individual  case  which  may 
present  itself. 

In  spite  of  its  apparent  complexity,  the  diagnosis  of  nervous  diseases  lends 
itself  better  than  that  of  the  diseases  of  most  of  the  other  organs  to  exact  path- 
ological analysis.  Just  as  a  chemist  in  analyzing  a  substance  of  unknown  com- 
position by  a  series  of  appropriate  tests  eliminates  from  consideration  one  group 
of  chemical  bodies  after  another  until  he  finally  discovers  its  class  and  name,  so 
the  neurologist  subjects  a  patient  to  one  test  after  another  iu  definite  sequence. 
As  the  result  of  each  test  he  throws  out  of  consideration  one  or  more  groups  of 
diseases  and  assures  himself  that  he  has  to  do  with  a  disease  belonging  to  another 
definite  group.     With  eaofa  successive  test   the  number  of  diseases  constituting 

a  group  becomes  less,  until  finally  one  definite  individual  disease  stands  revealed 
among  the  few  moai  closely  related  to  it  bya  comparison  of  the  remaining  symp- 
toms characteristic  of  each,  which  are  given  in  the  final  abstracts.  This  analyt- 
ical method  is  used,  I  think,  by  all  great  teachers  of  neurology  in  demonstrating 

cases  of  disease  before  their  classes  of  students.  It  is  the  crystallizat  ion  of  this 
teaching  into  the  tabular  form  which  this  book  attempts  to  present. 

In  using  this  book  for  diagnostic  purposes  it  is  important  that  the  "Intro- 
duction to  the  I tiagnostio  ( 'harts"  on  page  1 LQ  should  be  carefully  studied.  By 
means  of  these  charts  it  is  possible  to  diagnosticate  easily  and  rapidly  any  disease 


of  the  nervous  system  and  to  localize  the  lesion,  when  any  lesion  exists.  If  the 
examiner  makes  a  mistake  at  any  point,  the  next  step  in  the  process  or  the 
abstract  of  the  other  symptoms  of  the  disease  will  probably  show  him  that  he 
is  in  error  and  that  it  is  necessary  for  him  to  retrace  his  steps. 

For  the  sake  of  completeness  certain  trophic  diseases  are  included,  which, 
although  causing  a  number  of  functional  disturbances  in  the  nervous  system,  are 
not  really  nervous  diseases. 

As  might  naturally  be  expected,  the  same  disease,  in  so  far  as  it  presents 
many  symptoms,  appears  a  number  of  times  in  the  different  charts  and  even  in 
the  same  chart;  so  that,  in  order  to  get  a  more  complete  idea  of  its  symptoma- 
tology, it  is  essential  that  the  different  abstracts  of  it  should  all  be  read.  To 
facilitate  this,  cross  references  by  numbers  within  brackets  are  placed  in  the  text. 

Many  diagnostic  and  technical  terms  are  used  which  may  not  be  familiar 
to  the  student;  therefore  these  terms  are  classified,  defined  and  their  signifi- 
cance stated,  as  far  as  it  is  known  to  the  author,  in  a  series  of  semeiological 
charts  preceding  the  diagnostic  ones.  Cross  reference  to  these  terms  also  is 
facilitated  by  the  numbers  within  the  brackets.  A  very  full  index,  in  the  prepa- 
ration of  which  the  author  has  received  much  assistance  from  his  friend,  Dr. 
Dawes,  also  serves  this  same  purpose. 

The  peculiar  characteristic  of  this  book  on  diagnosis  is  that  it  gives  to  the 
student  or  physician  a  key  by  which,  in  a  comparatively  easy  manner  from 
one  or  more  important  symptoms,  he  can  arrive  at  a  diagnosis.  It  also  has  the 
advantage  that  it  divides  the  diseases  into  groups,  the  members  of  which  have 
a  definite  relationship  with  each  other;  so  that  in  the  process  of  using  the  charts 
the  student  is  constantly  catching  glimpses  of  the  natural  relationships  between 
the  different  diseases  of  the  nervous  system.  Although  the  symptoms  of  differ- 
ent diseases  have  often  been  contrasted  in  tables  of  parallel  columns,  in  no  other 
book,  known  to  the  author,  has  the  subject  been  presented  as  it  is  here,  and 
this  must  be  his  excuse  for  publishing  it  and  for  any  defects  which  it  may  show, 
as  there  was  no  model  which  could  be  followed  in  preparing  it. 

In  the  preparation  of  the  charts  the  author  has  received  valuable  sugges- 
tions and  aid  from  several  friends  and  especially  from  Drs.  Mosher,  Gordinier 
and  Archambault,  while  for  the  plates  he  is  greatly  indebted  to  Drs.  Streeter 
and  Hawn.  To  these,  his  present  friends  and  former  students  and  assistants, 
he  gratefully  acknowledges  his  indebtedness  and  returns  his  thanks. 

It  is  very  gratifying  to  the  author  that  the  first  edition  of  two  thousand 
copies  has  been  exhausted  in  eighteen  months,  giving  him  an  opportunity  of 
making  a  complete  revision  of  the  text,  and  of  adding  a  few  plates  and  also  intro- 
ductions both  to  the  semeiological  and  to  the  diagnostic  charts,  which  seem  to 
him  to  add  much  to  the  value  of  the  work. 

The  criticisms  of  Dr.  Mosher  and  his  untiring  aid  in  putting  both  editions 
through  the  press  are  large  factors  in  whatever  success  the  book  may  have. 

Henry  Hun. 

Albany,  N.  Y., 

August  1,  1914. 


PART  I 

SEMEIOLOGY 
THE  EXAMINATION  OF  PATIENTS 

AND  A 

PHYSIOLOGICAL  AND  PATHOLOGICAL  ANALYSIS 

OF  THE 

RESULTS  OBTAINED  FROM  SUCH  EXAMINATION 


AN  ANALYSIS  OF  THE 
SUBJECTIVE  AND  OBJECTIVE  SYMPTOMS  OF  DISEASE 


INTRODUCTION  TO  THE  SEMEIOEOGICAL  CHARTS 

The  diagnosis  of  nervous  diseases,  if  it  is  to  be  at  all  satisfactory  and  accurate,  must  be 
based  on  anatomy  and  physiology.  The  practitioner  is  supposed  to  have  some  acquaintance 
with  these  subjects,  and  the  curriculum  of  the  medical  college  is  so  arranged  that  the  student 
is  taught  them  before  he  commences  clinical  work.  It  seems,  however,  desirable  to  make  here 
an  attempt  to  present  a  brief,  but  comprehensive,  outline  of  the  physiology  of  the  nervous  sys- 
tem, including  some  statements  as  to  its  anatomy,  which  latter  can  be  supplemented  by  an  in- 
spection of  the  plates  at  the  end  of  the  book. 

The  fundamental  element,  or  unit,  of  the  nervous  tissue  is  the  neuron  (461-4)  a  cell  with 
many  processes  projecting  from  it;  some  short  and  branching  (dendrons),  one  (rarely  two)  which 
often  extends  a  long  distance  and  usually  becomes  the  axon  of  a  medullated  nerve  fiber,  and 
which,  in  some  cases,  gives  off  a  few  collateral  branches.  Both  axons  and  dendrons  are  com- 
posed of  delicate  fibrillae  which  pass  directly  without  interruption  through  the  cell  body.  Of 
these  neurons,  varying  in  form  and  size  and  supported  by  the  delicate  framework  of  the  neuro- 
glia, the  entire  nervous  system  is  composed. 

The  fundamental  physiological  characteristics  of  the  nervous  tissue  are  excitability  and 
transmission:  the  power  of  receiving  an  excitation  and  transmitting  it  from  one  end  of  the  neuron 
to  the  other  and  of  transmitting  it  to  other  neurons  with  which  the  first  is  in  anatomical  and 
physiological  relationship  or  contact.  By  its  dendrons  the  nerve  cell  receives  nervous  impulses 
and  by  its  axon  it  sends  out  its  own  impulses.  There  is  experimental  evidence  which  tends 
to  prove  that  the  activity  of  a  nerve  cell  is  the  result  of  chemical  reactions  (consumption  of 
rhromatophilic  substance,  etc.),  while  the  conduction  along  nerve  fibers  is  mainly  a  physical 
process.  The  transmission  of  energy  from  one  neuron  to  another  in  contact  with  it  serins  to 
depend  upon  differences  in  the  tension  of  this  energy  in  the  two  neurons.  The  cellular  activity 
is,  therefore,  easily  exhausted,  while  the  activity  of  the  nerve  fiber  is  not  easily  exhausted. 

Of  the  numerous  forces  and  forms  of  energy  in  the  world  only  a  portion  can  be  perceived 
by  man.  It  is  certain  that  some  animals  perceive  things  imperceptible  to  him.  The  various 
forms  of  energy  in  nature  cannot  act  directly  upon  the  nerve  to  produce  sensory  impulses,  but 
intermediate  organs,  "end-organs,"  are  necessary  to  transmute  the  external  energy  into  nervous 
energy.  In  virtue  of  chemical  changes  the  potential  energy  stored  in  the  end-organ  becomes 
active;  the  inciting  cause  of  this  being  the  external  or  foreign  irritation.  There  are,  doubtless, 
many  forms  of  energy  in  the  world  which  cannot  be  perceived,  because  there  are  no  suitable 
end-Organs  to  bring  aOOUl  this  transmutation.      Sometimes  this  can  lie  accomplished  by  adding 

to  the  end-organs  some  mechanical  contrivance  suitable  to  bring  about  this  transmutation;  as 

for  instance,  the  fluoroscopic  screen  for  X-rays.  The  universal  ether  is  doubtless  in  vibration 
far  beyond  the  limits  of  about  four  hundred  million  million  per  second,  which  constitute  for 
us  the  color  red,  and  about   seven  hundred  and  sixty  million  million,  which    constitute    violet; 

and  indeed  we  have  reason  to  believe  thai  the  ultra-violet  rays  have  some  effect  upon  our  body, 

but  beyond  the  above  limits  the  vibrations  of  the  ether  are  not  recognizable  by  our  eye  and 
brain.      The  absence  of  a  sensory  end-organ  limits  the  number  of  perceptions  and  consequently 

the  content  of  consciousness,  but  this  content  is  or  can  be.  much  larger  at  the  present  time 
than  in  times  past.  Many  new  forces  I  X-ray,  etc.)  are  now  perceptible  by  the  organs  of  -m-e 
which  were  before  itipercept ible.  The  seti-ory  apparatus  also  is  not  absolutely  perfect.  Things 
moving  very  rapidly  cannot  be  seen.      The  -poke-  of  a  rapidly  revolving  wheel  cannot   be  -,  ,  n 


The  Origin  and  Transmission  of  Sensory  Impulses 

Cutaneous  and  muscle-joint  sensation  (Chart  Via).  The  surface  of  the  body  and  the  cavi- 
ties connected  with  it  contain  organs:  the  terminal  organs  of  sense  (the  sensory  "end-organs"), 
which  bring  the  body  into  connection  with  some,  but  probably  far  from  all,  of  the  forces  of 
nature,  and  which  "end-organs"  are  so  constructed  as  to  transmute  physical  forces  (light  in 
the  eye;  sound  in  the  ear;  heat,  cold,  touch,  pressure  and  pain  in  the  skin,  etc.)  into  nervous 
excitations  in  the  terminal  filaments  of  the  peripheral  nerves.  The  skin  contains  many  of 
these  isolated  terminal  sense  organs  and,  therefore,  sensibility  is  not  spread  uniformly  over  the 
skin,  but  is  located  in  individual  points.  From  these  points  of  greatest  sensibility,  its  acuteness 
diminishes  concentrically.  In  every  square  centimeter  of  skin  there  are,  on  the  average,  12  to 
13  points  for  cold,  0  to  3  for  heat,  and  24  for  pressure,  impressions;  although  these  figures  vary 
very  greatly  for  different  parts  of  the  skin,  the  points  being  most  numerous  on  the  finger  tips 
and  fewest  on  the  back.  Most  observers  maintain  that  there  are  distinct  points  also  for  pain- 
ful sensibility.  Where  the  skin  is  stretched  over  bone  (the  malleoli),  sensation  is  less  distinct 
and  is  more  distinct  where  the  skin  is  hairy;  a  point  for  tactile  sensibility  being  situated 
at  the  base  of  most,  if  not  of  all,  hairs.  There  may  be  a  delay  of  several  seconds  in  the  conduc- 
tion of  painful  impressions,  and  there  may  be  a  summation  of  painful  impressions;  so  that  with 
repeated  pin-pricks  the  pain  becomes  more  acute.  After  section  or  injury  of  a  nerve,  the  anes- 
thesia and  analgesia  are  never  so  extensive  as  is  the  area  of  distribution  of  the  nerve,  and  sensi- 
bility often  returns  before  the  regeneration  of  the  nerve  has  taken  place.  This  is  partly  due 
to  peripheral  anastomoses  and  partly  to  recurrent  fibers  of  the  sensory  nerve. 

Head  and  his  colleagues,  after  much  experimental  work  on  the  subject,  arrived  at  the  fol- 
lowing conclusions: 

There  are  in  the  peripheral  areas  three  kinds  of  sensibility,  due  to  there  being  three  different 
kinds  of  nerve  fibers  supplied  to  each  area. 

1st.  Deep  Sensibility.  Muscle  sense,  pressure  sense,  pressure  pain  and  localizing  sense. 
This  sensibility  is  conveyed  by  sensory  nerve  fibers,  more  or  less  deeply  situated,  beneath  the 
skin  and  usually  running  with  the  motor  nerves.  When  the  motor  nerves  of  the  muscle  tendons 
are  cut,  these  forms  of  sensibility  are  lost. 

2nd.  Epicrilic  Sensibility.  Tactile  sensibility  for  slight  impressions,  form  and  space  sense, 
sense  of  moderate,  not  extreme,  temperatures  (22°  to  40°  C.)  and  the  precise  localization  of  pain 
and  temperature  sense.  This  area  of  sensibility  is  very  constant  for  each  individual  nerve. 
The  restitution  of  this  form  of  sensibility  is  very  slow  and  is  not  complete  until  after  several  years. 

3rd.  Protopathic  Sensibility.  Pain  and  sense  of  extremes  of  temperature  (below  22°  or 
above  40°  C).  These  symptoms  are  accompanied  by  paresthesiae  and  a  false  localization. 
This  form  of  sensibility  is  best  tested  on  the  periphery  of  the  affected  area,  where  the  anesthesia 
is  not  complete,  or  over  the  whole  area  while  regeneration  is  taking  place.  The  restitution  of 
this  form  of  sensibility  is  relatively  rapid  (7  to  10  weeks). 

These  researches  of  Head  are  of  great  interest  and  value  and  have  attracted  much  atten- 
tion and  discussion,  but  they  are  not,  in  their  entirety,  accepted  by  all  neurologists. 

Sensory  impulses  of  all  kinds  are  carried  to  the  central  nervous  organs  by  the  sensory  nerves. 
Of  these,  the  spinal  enter  the  cord  through  their  cell  bodies  in  the  spinal  ganglia  and  through  the 
posterior  nerve  roots  (Fig.  26) ;  while  the  fibers  of  the  trigeminal,  the  great  cranial  nerve  supply- 
ing sensation  to  the  face,  after  passing  through  their  cell  bodies  in  the  Gasserian  ganglion,  enter 
the  trigeminal  sensory  nucleus  in  the  pons  (Fig.  19).  The  fibers  from  the  posterior  nerve  roots, 
on  entering  the  spinal  cord,  are  sorted  according  to  their  physiological  function  into  three  great 
parts  (Fig.  26).  One  part,  which  conveys  tactile,  pressure  and  muscle-joint  sense  impressions, 
ascends,  mainly  without  decussating,  in  the  posterior  columns  to  the  nuclei  of  the  columns  of 
Goll  and  Burdach,  and  thence  is  continued  by  a  new  set  of  neurons  (the  internal  arcuate  fibers), 
which  decussate  and  pass  through  the  median  lemniscus  (Figs.  20-3)  to  the  optic  thalamus, 
whence  it  is  continued,  also  by  another  set  of  neurons  (relays),  to  the  parietal  cortex.  The  second 
part,  which  conveys  impulses  for  co-ordination,  passes  to  the  cells  of  the  column  of  Clarke  and 

6 


thence,  mainly  without  decussating,  through  the  direct  cerebellar  tract  in  the  outer  part  of 
the  lateral  column  and  through  the  restiform  body  to  the  cerebellum.  The  third  part,  which 
conveys  temperature  and  painful  impressions,  passes  through  cells  in  the  posterior  horn,  decus- 
sates in  the  central  gray  matter  of  the  cord  and  passes  upward  in  the  antero-lateral  column 
through  the  spino-thalamic  tract  and  lateral  portion  of  the  formatio  reticularis  to  the  optic 
thalamus,  and  thence  to  the  cortex. 

A  destructive  lesion  either  in  the  terminal  end-organ,  or  at  any  point  of  these  sensory  tracts 
or  neurons,  causes  a  corresponding  paralysis  of  sensation  (anesthesia);  while  a  slight,  irritative 
lesion  may  cause  hyperesthesia,  paresthesiae  or  pain  in  the  distribution  of  the  nerve. 

In  addition  to  the  anesthesia,  which  occurs  in  organic  disease  ot  the  nervous  system,  there 
is  an  anesthesia  which  occurs  in  hysteria:  hysterical  anesthesia.  This  hysterical  anesthesia, 
occasionally  but  rarely,  involves  the  organs  of  special  sense.  It  more  commonly  involves  cu- 
taneous sensibility  and  then  the  anesthesia  is  not  limited  to  the  distribution  either  of  a  peripheral 
nerve  or  of  a  nerve  root.  It  may  instantaneously  disappear.  It  may  recur  in  the  same  place, 
or  in  some  other  locality.  It  does  not  prevent  the  use  of  the  part  in  performing  acts,  in  which 
sensibility  is  essential.  Upon  excitation  of  the  anesthetic  parts  vascular  reflexes  occur,  which 
is  never  the  case  in  anesthesia  due  to  organic  disease,  peripheral  or  spinal.  It  is  evident  that 
this  hysterical  anesthesia  is  the  result  of  imagination  or  delusion.     It  is  purely  psychic. 

Pain  (374)  is  an  unpleasant  sensation  which  never  occurs  in  health,  but  only  when  the 
body  is  injured,  either  mechanically  or  chemically.  It  is  a  signal  of  warning  that  the  body 
needs  protection.  Its  intensity  depends  not  only  upon  the  intensity  of  the  mechanical  or  chem- 
ical irritation,  but  also  upon  the  condition  (inflammatory,  etc.)  of  the  peripheral  nerves  and 
of  the  cerebral  cortex.  It  is  more  intense  when  accompanied  by  fear  and  apprehension.  An 
unexpected  wound  is  less  painful  than  an  anticipated  one.  Pain  is  often  associated  with  the 
allied  perceptions  called  ''paresthesiae"  (375)  which  at  times  precede,  at  times  accompany, 
and  at  times  follow,  the  pain,  and  which  are  usually  of  central  origin  and  are  due  to  irritation 
of  the  sensory  fibers  at  some  part  of  their  course  through  the  central  neivous  organs. 

Gustatory  sensation  (Chart  Via).  The  mucous  membrane  of  the  mouth  (in  addition  to  the 
terminal  organs  for  tactile,  pressure,  thermic,  painful,  etc.,  impressions)  contains  also  the  term- 
inal organs  of  the  nerves  of  taste:  the  taste  buds  or  bulbs,  so  called  from  their  form,  embedded 
in  the  epithelium  of  the  mucous  membrane  of  the  mouth,  especially  of  the  tongue.  Excitation 
of  these  taste  bulbs  gives  rise  to  four  distinct  gustatory  sensations:  sweet,  acid,  salty  and  bitter, 
to  which  may,  perhaps,  be  added  alkaline  and  metallic.  Many  so-called  tastes  are  really  a 
combination  of  gustatory  and  olfactory  sensations.  The  nerve  fibers  arising  from  the  taste 
bulbs  on  the  posterior  portion  of  the  tongue  pass  by  the  glosso-pharyngeus  nerve  in  a  direct 
miumer  through  the  petrous  ganglion  to  its  nucleus  in  the  medulla,  whence  they  ascend  with 
the  other  sensory  fibers  of  the  lemniscus  to  the  optic  thalamus,  and  thence  to  the  cerebral  cortex 
posterior  to  the  gyrus  hippocampi  (Fig.  Hi);  while  the  nerve  fibers  arising  from  the  taste  bulbs 
On  the  anterior  portion  of  the  tongue  pass  at  first  in  the  lingual  nerve  and,  soon  leaving  this. 
form  the  chorda  tympani,  which  joins  the  facial  nerve  and  runs  with  it  through  the  fallopian 
canal  to  the  geniculate  ganglion.  Here  the  fillers  divide;  a  pari  continuing  alongside  the  facial 
nerve  and  forming  the  nervus  intermedins,  which  runs  to  a  nucleus  in  the  medulla  dose  to  the 

glosso-pharyngeal  nucleus;  while  the  reel  of  the  fibers  run  through  the  petrosal  nerves  and  join 
the  fifth  nerve  and  pass  to  the  Qasserian  ganglion  (Fig.  38),  ami  thence  to  the  cerebral  cortex 

ii'n.      A    destructive   lesion   at    any   point    of   this   course   will   cause   unilateral   loss  of  taste 

ia).    When  the  lesion  is  in  the  Fallopian  canal  tl  maj  be  associated  with  facial 

paralysis  on  the  same  side. 

Olfactory  ttntaUon  (than  Via).  The  mucous  membrane  of  the  nose,  analogous  to  that 
of  the  mouth  (in  addition  to  the  terminal  organs  for  tactile,  thermic,  pressure,  painful. 
impressions),  contains  also  the  terminal  organs  of  the  nerves  of  smell.  The  nerves  terminating 
in  these  ornan-  pass  upward  through  the  cribriform  plate  t<>  the  olfactory  bulb,  ami  thence  back- 
ward through  the  olfactory  tract:  some  to  the  anterior  perforated  space  and  Bub-thalamic  region 


(olfactory  reflexes)  and  some  to  the  cortical  center  for  smell  in  the  gyrus  hippocampi  (olfactory 
perceptions)  (Fig.  16).  Each  olfactory  bulb  is  connected  through  the  anterior  commissure 
with  both  cortical  centers. 

Hearing  (Chart  Via.)  The  terminal  organ  for  hearing  is  the  organ  of  Corti  in  the  cochlea, 
within  the  petrous  portion  of  the  temporal  bone.  In  this  organ  there  is  a  long  series  of  vibratory 
structures  of  unequal  lengths;  so  that  on  them  can  be  reproduced  every  possible  tone  with  its 
over-tones  or  harmonics.  The  auditory  nerves  terminating  in  this  organ  pass  to  the  ventral  and 
dorsal  auditory  nuclei  in  the  pons.  From  these  nuclei  fibers  pass  upward,  some  decussating  and 
some  not,  through  the  lateral  fillet  to  the  corpora  quadrigemina,  and  thence  through  the  sub-lenti- 
cular region  of  the  internal  capsule,  posterior  to  the  fibers  for  cutaneous  sensibility,  and  reach  the 
cortical  auditory  center  in  the  anterior  part  of  the  superior  temporal  convolution  (Fig.  15).  A 
destructive  lesion  of  one  auditory  nerve  will  cause  unilateral  deafness  on  the  same  side,  but  a 
lesion  of  the  tract  connecting  the  sub-cortical  with  the  cortical  centers,  since  this  tract  con- 
tains both  crossed  and  uncrossed  fibers,  will  not  cause  any  deafness.  Deafness  results  only 
from  a  bilateral  central  lesion  affecting  the  corpora  quadrigemina  or  the  sub-cortical  tracts 
described  above.  Even  destruction  of  the  auditory  cortical  center  in  both  hemispheres  does 
not  seem  to  cause  complete  deafness. 

Sight  (Chart  Via).  The  terminal  organs  for  sight  are  the  rods  and  cones  in  the  retina  within 
the  eyeball.  The  rods  seem  to  be  concerned  in  seeing  in  dim,  the  cones  in  bright,  light.  They 
vary  in  relative  numbers  in  different  animals,  according  as  they  roam  by  night  or  by  day.  From 
these  structures  start  the  terminal  filaments  of  the  optic  nerves,  which  run  backward  from  the 
eyeballs.  In  the  optic  chiasm  the  fibers  from  both  maculae  luteae  and  from  the  nasal  half  of 
each  retina  decussate;  so  that  in  the  left  optic  tract  are  collected  all  the  fibers  from  the  left  half 
of  each  retina  (right  visual  field)  and  those  from  both  maculae  luteae;  while  in  the  right  optic 
tract  are  collected  all  the  fibers  from  the  right  half  of  each  retina  (left  visual  field)  and  those 
from  both  maculae  luteae.  The  fibers  of  the  optic  tract  on  each  side  terminate  in  the  external 
geniculate  body,  the  pulvinar  and  the  anterior  quadrigeminal  body  of  the  same  side,  and  are 
thence  continued  through  the  posterior  portion  of  the  internal  capsule  and  the  fasciculus  of 
Gratiolet  to  the  lips  of  the  calcarine  fissure  on  the  median  surface  of  the  occipital  lobe  of  the 
same  side  (Fig.  37). 

A  destructive  lesion  of  the  optic  nerve  causes  blindness  of  the  corresponding  eye,  but  a  lesion 
of  any  portion  of  the  optic  tract,  or  geniculate  body,  or  fasciculus  of  Gratiolet,  or  of  the  lips  of 
the  calcarine  fissure  will  cause  homonymous  hemianopia  of  the  field  of  vision  of  the  opposite 
side;  while  a  lesion  of  the  central  portion  of  the  optic  chiasm  will  cause  binasal  hemianopia. 

Internal  or  general  sensation.  In  addition  to  these  sensory  impulses  which  convey  to  the 
brain  excitations  from  the  special  sensory  organs  and  hence  from  the  external  world,  there  are 
others  which  come  from  the  different  organs  of  the  body  and,  in  case  they  reach  the  cortex,  give 
rise  to  what  is  called  internal  or  general  sensation.  Some  of  these  internal  excitations  remain 
entirely  peripheral  and  affect  mainly  the  blood  vessels;  others  reach  no  further  than  the  spinal 
cord  or  ganglia  at  the  base  of  the  brain  and  incite  those  automatic  acts  which  preserve  the  nutri- 
tion and  the  life  of  the  individual;  while  others  reach  the  cerebral  cortex  and  at  times  affect 
profoundly  the  processes  taking  place  in  it.  These  general  sensations  have  much  influence  on 
a  person's  emotions,  moods,  thoughts  and  actions.  Hunger  may  entirely  alter  the  normal 
acts  of  a  man  or  beast. 

Such  internal  or  general  sensations  are  for  the  most  part  ill-defined  and  ill-localized.  They 
seem  to  depend  upon  the  blood  supply  and  upon  the  activity  of  the  different  organs  and  upon 
the  state  of  contraction  of  the  hollow  organs;  and  they  appear  to  have  much  to  do  with  our 
feeling  of  comfort  or  discomfort,  which  latter  may  amount  to  even  severe  pain.  The  sensation 
of  hunger  seems  to  be  caused  by  contraction  of  the  empty  stomach,  and  the  various  colics  by 
contraction  of  the  circular  muscular  fibers  of  the  intestine,  the  ureter  or  the  bile  duct.  But 
the  best  understood  of  all  these  internal  or  general  sensations  is  the  composite  one  called  muscle- 
joint  sense,  which  is  mainly  made  up  of  impulses  from  the  muscle  and  its  tendon  and  the  articu- 

8 


lating  surfaces  and  also  from  impulses  from  the  skin  and  other  tissues  in  the  neighborhood, 
as  these  are  stretched  or  relaxed  in  motions  of  the  joint.  The  muscle-joint  sensory  conduction 
we  have  already  considered  in  connection  with  the  conduction  of  tactile  sensory  impulses.  To 
these  internal  sensations  must  be  added  also,  probably,  the  cortical  innervation  feelings  (see 
later)  inasmuch  as  a  person  often  feels  that  he  is  moving,  or  feels  that  he  knows  the  position 
of,  a  paralysed  or  even  amputated  limb. 

Sensation  (Chart  VI) 

When  these  various  impulses  have  passed  along  the  various  tracts  and  have  traversed,  and 
been  interrupted  by,  several  masses  of  gray  matter,  they  reach  the  sensory  area  of  the  cerebral 
cortex  and  there  give  rise  to  a  new  form  of  energy  called  sensation.  That  is  to  say,  a  physical 
force  (as  for  instance,  ether  in  rapid  undulation)  is  converted  in  a  terminal  organ  into  nervous 
energy,  and  as  such,  having  traversed  the  sensory  tracts,  reaches  the  cerebral  cortex.  It  is 
there  transmuted  into  a  new  form  of  energy  (as  for  instance  the  sensation  of  light).  The  sen- 
sation of  light  takes  place  in  the  brain,  not  in  the  eye,  and  has  no  similarity  to  the  undulations 
of  ether  from  which  it  normally  originates,  and  it  may,  indeed,  be  caused  not  only  by  these,  but 
also  may  originate,  in  perfect  darkness,  from  mechanical  irritation  of  the  eye  (as  by  pressure 
from  the  finger  upon  the  eyeball)  or  of  the  optic  nerve.  Sensation  is,  therefore,  rather  a  symbol 
than  a  picture  of  the  external  object,  with  which  by  experience  it  is  associated. 

Sensation  is  thus  a  special,  individual  force,  similar  to  electricity,  light,  etc.,  which  is  pro- 
duced in  the  cerebral  cortex  and  which  has  its  special,  individual  characteristics.  A  complex 
manifestation  of  this  force  constitutes  consciousness  and  personality.  Sensations  originating 
from  the  different  organs  of  sense  are  located,  as  we  have  seen,  in  different  and  special  portions 
of  the  cortex  (Figs.  15  and  16)  and  do  not  at  all  resemble  the  external  phenomena  causing  them. 
A  clap  of  thunder  and  a  flash  of  lightning  are  very  different  external  phenomena,  but  the  reac- 
tions in  the  cortex,  which  constitutes  these  sensations,  probably  vary  in  topography  rather  than 
in  quality.  We  know  nothing  more  of  the  essence  of  this  form  of  energy,  which  we  call  sensa- 
tion, than  we  do  of  the  essential  nature  of  electricity,  or  of  contractility  in  the  muscle  fiber 
or  in  the  amoeba.  We  know  something  of  its  effects  and  we  know  something  of  the  locality 
of  the  cerebral  cortex  in  which  it  occurs  (Figs.  15  and  16)  and  that  it  is  very  dependent  upon 
abundant  blood  supply  and  that  it  must  result  from  chemical  actions  taking  place  in  the  cortex. 
Conscious  sensation,  probably  occurs  only  in  those  animals  which  possess  cerebral  hemispheres. 

Sensation  and  all  other  forms  of  mental  activity  are  absolutely  dependent  upon  a  fairly 
healthy  cerebral  cortex  and  a  fairly  abundant  blood  supply  to  it.  When  the  cerebral  hemis- 
pheres in  an  animal  are  removed,  or  when  the  cerebral  cortex  in  man  is  entirely  or  mainly  destroyed 
by  disease,  OX  in  B  child  the  hemispheres  are  absent  or  very  defective,  or  when  the  blood  supply 
is  cut  off  from  the  cerebral  cortex  altogether  or  in  large  part,  then  sensation,  perception,  memory, 
thought,  emotion  (and  its  corporeal  expression),  ethics,  association  of  ideas,  voluntary  motion, 
inhibition,  intelligence,  personality  and  consciousness  are  all  lost. 

Sensation  is  the  simplest  manifestation  of  consciousness  (see  later)  or  cognition.  For  its 
production  a  certain  degree  of  intensity  of  the  nervous  impulses  is  essential,  below  this  point 
of  intensity  the  cortex  may  be  in  activity,  but  sensation  will  not  result;  the  activity  will  be 

sub-conscious,    A  series  of  these  alight  impulses  quickly  repeated  may  by  summation  cause 

sensation.  There  is,  therefore,  a  minimum  of  intensity  necessary  for  sensation;  jusl  a-  elec- 
tricity passing  through  a  wire  must  have  a  certain  intensity  before  the  wire  glows  and  lighl  IS 
produced.  There  is  also  a  maximum  beyond  which,  no  matter  how  great  the  irritation,  then 
is  no  increase  of  sensation,  hut  rather  a  diminution  from  exhaustion  of  the  nerve  cell-.  Between 
(hi-  minimum  and  maximum  point,  sensibility  increases,  or  diminishes,  not  continuously,  hut 
by  little  steps;  a  definite  ratio  to  the  stimulus  (Weber's  law). 

furthermore,  a  weak  or  moderately  strong  excitation  may  reach  the  cortex  at  a  time  when 
other  portions  of  the  cortex  are  in  such  strong  excitation  that  this  weak  irritation  may  produce 

no  sensation,  but  remain  Bub-oonsdous.    The  line  between  the  oonsoioufl  and  the  sub-conscious 

cannot   be  sharplv  drawn. 

9 


Perceptions  and  Concepts  (Chart  VI) 

A  perception  consists  of  a  combination  of  sensations,  which  are  obtained  from  various  sen- 
sory end-organs,  but  all  of  which  proceed,  usually  simultaneously,  from  the  same  external  object. 
A  perception  of  an  apple  is  composed  of  several  sensory  impulses:  of  visual  sensations  from  the 
retina,  representing  the  outline  and  markings  and  color  of  the  apple;  of  muscle  sensation  from 
the  ocular  muscles,  representing  its  distance  from  the  e}re,  its  position  in  relation  to  other  objects 
and  to  some  extent  its  form;  of  tactile  sensations  from  the  hand,  representing  its  form,  firmness 
and  texture;  and  of  gustatory  sensations  from  the  mouth,  representing  its  taste.  The  various 
physico-chemical  changes,  thus  set  in  aetivitj-  in  the  cortex,  combine  to  produce  the  full  percep- 
tion of  the  apple.  For  a  full  and  complete  perception,  consisting  as  it  does  of  so  many  elemen- 
tary sensations,  quite  an  appreciable  time,  or  frequent  repetition,  is  needed.  The  development 
of  a  perception  is  found  by  experiment  to  proceed  from  generalities  to  details.  A  combination 
of  the  full  perceptions  of  many  apples,  each  resembling  and  at  the  same  time  in  some  respects 
differing  from  the  other,  produces  the  idea  or  concept  of  an  apple,  with  which  is  associated  its 
written  and  spoken  name  and  any  other  experiences  or  knowledge  which  have  become  asso- 
ciated during  our  life  with  apples.     (See  also  under  Associations.) 

Perceptions  occur  in  the  cerebral  cortex  in  immediate  proximity  to  the  cortical  termination 
of  the  corresponding  projection  fibers.  Each  cortical  center  consists  of  a  smaller  portion,  in  which 
the  projection  fibers  terminate  and  a  larger  portion,  in  which  perceptions  take  place  and  in  which 
their  memories  are  stored.  Thus,  the  optic  fibers  terminate  in  the  lips  of  the  calcarine  fissure, 
while  the  rest  of  the  median  and  convex  surface  of  the  occipital  lobe  is  devoted  to  optical  percep- 
tions and  memories  (Figs.  15  and  16).  When  sensations  only,  but  not  perceptions,  can  occur,  as 
when  that  portion  of  the  center  in  which  the  projection  fibers  do  not  terminate  is  diseased,  the 
condition  is  called  in  general  agnosia.  When  there  is  a  failure  of  tactile  perceptions  the  condition 
is  called  astereognosis;  in  failure  of  optical  perceptions  soul-blindness,  or  psychic  blindness,  and  in 
failure  of  auditor}'  perceptions  soul-deafness,  or  psychic  deafness,  or  auditory  or  sensory  aphasia. 
When  that  portion  of  the  cortex  in  which  the  sensory  fibers  terminate  is  diseased,  both  percep- 
tion and  sensation  are  abolished. 

Emotions  (Chart  III) 

Certain  activities  of  the  brain  are  accompanied  by  feelings  of  pleasure  or  discomfort  or 
even  pain,  and  usually  also,  if  these  feelings  are  moderately  intense,  by  changes  in  the  func- 
tional activity  of  the  internal  organs,  especially  in  the  circulatory  and  respiratory  systems, 
but  also  in  the  alimentary  canal  and  in  the  other  viscera  and  glands  of  the  body.  These  feel- 
ings are  due  in  great  part  to  the  internal  or  general  sensations.  When  the  bodily  functions  are 
disordered  we  have  a  general  feeling  of  discomfort  and  when  all  is  working  well  we  have  a  sense 
of  buoyancy  and  exaltation;  all  moves  smoothly  without  friction,  as  in  a  well  oiled  machine. 
These  internal  sensations,  as  was  mentioned  on  a  previous  page,  are  ordinarily  the  dominant  factor 
in  our  feelings  and  emotions  and  greatly  influence  also  our  voluntary  actions,  which  for  instance 
may  be  altogether  different  in  a  state  of  hunger  from  those  in  a  state  of  satiety.  Indeed  the 
internal  sensations,  such  as  hunger,  etc.,  are  very  often  themselves  the  cause  of  extensive  vol- 
untary acts,  which  have  for  their  aim  relief  from  this  sensation.  As  these  internal  sensations 
vary  from  time  to  time,  our  moods  change,  and  perceptions,  which  at  one  time  are  pleasant, 
may  at  another  time  be  unpleasant.  Irrespective  of  our  moods,  however,  some  perceptions 
are  almost  always  pleasant,  others  are  not.  Things  which  tend  toward  the  preservation  and 
health  of  one's  self  and  his  family  are  usually  pleasant,  and  vice  versa.  Perceptions  to  which 
we  have  become  accustomed  are  usually  pleasant,  and  even  unpleasant  perceptions  by  frequent 
repetition  at  times  become  bearable  and  even  pleasant. 

Not  a  few  perceptions  are  accompanied  with  relief  of  discomfort,  as  when  hunger  is  assuaged, 
or  we  accomplish  something  desired  or  in  some  way  contribute  to  our  well-being  or  success  and 
thus  give  pleasure;  while  other  perceptions  act  in  a  contrary  manner.  These  feelings  of  pleasure 
and  pain  may  be  due  in  part  to  the  intensity  of  the  sensation  or  perception,  in  part  to  heredity, 
as  a  result  of  evolution  in  case  of  objects  desirable  for  the  health  of  the  body;  but  in  greater  part 

10 


to  associations  (see  Associations)  with  previous  similar  perceptions,  and  in  greatest  part  with 
the  feeling  of  satisfaction  or  dissatisfaction  with  the  result  of  one's  actions. 

Sensations  of  moderate  intensity  are  usually  pleasant;  while  sensations  of  very  great  in- 
tensity, which  produce  abnormally  strong  reactions  in  the  nervous  tissue,  are  usually  unpleas- 
ant. Sensations  originating  from  sets  of  vibrations  having  a  simple  ratio  to  each  other  are 
usually  pleasant,  while  those  which  have  a  complicated  ratio  are  usually  unpleasant.  Foods 
which  nourished  our  ancestors  usually  taste  good  to  us.  The  child  probably  acquires  a  taste 
for  sweet  things  from  the  sugar  in  its  mother's  milk.  Most  of  our  pleasant  and  unpleasant 
sensations  arc  the  result  of  our  education.  They  are,  therefore,  much  more  pronounced  in 
adults,  especially  educated  ones,  than  they  are  in  children.  A  perception  which  is  associated 
with,  or  followed  by,  pleasure  or  pain  will  always,  or  for  a  long  time,  as  often  as  it  occurs  actually 
or  in  memory,  be  accompanied  by  a  pleasant  or  painful  emotion,  whether  the  memory  of  the 
original  pleasant  or  painful  result  associated  with  it  is  present  in  consciousness  or  not. 

Mankind  does  not  find  itself  in  this  world  with  all  its  needs  and  wants  satisfied;  on  the  con- 
trary everyone  must  acquire  food,  clothes,  habitation,  warmth  and  a  hundred  other  necessi- 
ties. A  man  who  sees  his  neighbor  with  something  good,  which  he  has  not,  desires  it,  or  some- 
thing similar.  These  wants  and  desires  are  the  great,  almost  the  only,  incentives  to  voluntary 
action.  When  this  voluntary  action  results  in  success  we  have  in  it  our  greatest  pleasure  and 
when  it  results  in  failure,  our  greatest  unhappiness.  All  things  connected  with  our  success 
receive  an  associated  emotion  of  happiness;  while  those  things  connected  with  our  failure  receive 
an  associated  emotion  of  grief. 

In  these  various  ways  a  certain  number  of  our  perceptions  have  associated  with  them  an 
emotion  (204),  or  tone,  of  pleasure  or  pain,  greater  or  less,  and  a  series  of  such  emotions,  or  one 
long  continued,  will  make  us  happy  or  unhappy  for  a  considerable  length  of  time  and  will  con- 
stitute what  we  call  our  "mood." 

In  certain  abnormal  states  of  the  cerebral  cortex  (exhaustion,  circulatory  irregularities, 
poison  and  other  less  well  known  disorders)  the  emotions  become  dissociated  from  the  ideas 
with  which  they  are  normally  associated;  so  that  all  cerebral  activity  is  accompanied  by  one 
emotion;  in  some  cases,  sadness;  in  others,  fear;  in  others,  joy  and  in  others  apathy  or  absence 
of  all  emotion.  An  emotion  is  often  so  strong  and  so  occupies  the  patient's  consciousness  thai 
it  is  impossible,  or  nearly  so,  to  attract  his  attention. 

Memory   I  (  'mart  III) 

When  perceptions  take  place,  chemical  changes  are  occurring  in  a  definite  portion  of  the 
cerebral  cortex,  which  not  only  produce  the  perception,  but  also  leave  thereafter  a  permanent 

alteration  in  the  cortex.  The  force  derived  from  tin-  chemical  changes  taking  place  in  the 
cortex  during  an  active  perception  may  n^ult  in  a  structural,  physical  or  chemical  change  in 
the  nervous  element-,  or  more  likely  in  the  storing  in  them  of  potential  energy,  which  can  lie 
liberated  and  become  actual  later.  Memories  are  dynamic  changes  in  nerve  cells  and  fibers 
which    reduce    the    resistance    to   subsequent    similar    impressions   or   excitations.      Certainly,    a 

definite  change  is  brought  about  which  registers  a  permanent  memory  of  the  object  perceived 

and    subsequently   this   memory   can    be   latent    (sub-COnscioUS),  OT  active  (cOUBCioUs),  from  time 

to  tune.  Consciousness,  the  actual  perception  of  an  object  and  its  associated  active  memories 
(active  attention), is  a  very  exhausting,  energy  consuming  process  for  the  cerebral  cortex.  Bub* 
consciousness1    the  preservation   of  memories,  not   present  in  consciousness,  is  not  exhausting 

to  the  cortex,  even  though  1  he  memories  be  preserved  tor  many  years. 

In  virtue  of  this  change  in  the  cortex,  a  memory  of  tin-  perception  always  results  from 

irritation  of  this  altered  cortex.  This  memorv  ma\  l>e  arOUSed,  or  enter  into  munition,  by  the 
external   force   which   originally   caused   it    and,    I  hen.   the  object    will   be    rfnujriizr.l    i  re-kno\vn ), 

because  'he  actual  perception  cone-ponds  perfectly  with  its  memory;  or  the  memory  may  be 
aroused  by  way  of  those  association  fibers  which  it  had  previously  set  into  activity.  Memories 
become  associated  with  each  other  In  accordance  with  the  relationship  of  the  objects  causing 

11 


them,  as  the  result  of  our  experiences  with  these  objects.  In  perception,  then,  a  trace  of  the 
cortical  excitation  remains  in  the  cerebral  cortex  as  a  memory,  in  a  sense  analogous  to  the  per- 
sistence and  after  image  in  the  retina  after  strong  excitation  (looking  for  some  time  at  a  bright 
light). 

These  memories  are,  however,  very  different  qualitatively  from  the  original  perceptions. 
The  former  have  no  actuality.  Even  though  they  may  be  at  times  very  vivid,  they  never  seem 
real  to  a  normal  personality. 

The  whole  cortex  of  the  brain  is  in  great  part  a  huge  store-house  of  memories.  These 
memories  are  grouped  together;  so  that  those  which  are  derived  from  the  same  organ  of  sense 
lie  together  in  the  cortex.  This  localization  of  memories  has  been  worked  out  with  great  care 
and  is  to  a  considerable  extent  known.  It  is  shown  in  Figs.  15  and  16.  A  local  cortical  lesion 
may  thus  produce  a  loss  of  a  group  of  allied  memories. 

All  memories  are  sensory  in  character  with  exception  of  one  doubtful  group.  This  group 
consists  of  memories  of  so-called  "innervation  feelings."  When  a  muscle  is  contracted  the 
person  to  whom  it  belongs  has  a  feeling  of  this  contraction  and  can  estimate  its  strength.  This 
feeling  in  called  an  "  innervation  feeling  "  and  its  memory  is  stored  away  in  the  cortex  of  the 
anterior  central  convolution  and  of  the  neighborhood  in  front  of  it.  This  innervation  feeling 
seems  to  be  essential  for  the  voluntary  performance  of  the  corresponding  act.  When,  in 
consequence  of  a  cortical  brain  lesion  in  the  area  in  which  these  memories  are  stored,  a  person 
loses  the  power  of  performing  certain  acts,  he  often  says,  "  I  have  forgotten  how  to  do  it."  These 
innervation  feelings  and  memories  do  not  obtrude  themselves  strongly  into  our  consciousness. 
They  have  rather  to  be  sought  for,  but  they  usually  can  be  observed,  except  in  those  actions 
which  follow  very  rapidly  upon  the  perception,  or  memory,  causing  them.  There  are  many 
physiologists  and  psychologists,  however,  who  question  whether  there  are  any  so-called  inner- 
vation feelings  or  memories  in  consciousness.  However  that  may  be,  whether  true  innervation 
memories  exist  or  not,  the  function  of  this  cortical  area  is  an  actuality  and  whenever  a  portion 
of  the  motor  cortex  is  sufficiently  excited  by  a  perception,  or  a  memory,  from  the  sensory  cor- 
tex, a  so-called  voluntary,  or  association,  action  results.     (See  Voluntary  Movements.) 

Association 

The  essential  physiological  characteristics  of  nervous  tissue  are:  first,  its  excitability,  its 
reaction  to  stimulation  by  the  discharge  of  nervous  energy  stored  within  it;  and  second,  its 
transmissibility,  this  nervous  energy,  whenever  produced,  does  not  long  remain  localized,  but 
tends  to  pass  along  nerve  fibers,  throughout  its  own  neurons  and  to  other  neurons.  The  chan- 
nels along  which  it  will  pass  depend  upon  the  anatomical  arrangement  of  the  fibers.  In  con- 
sequence of  heredity  and  evolution,  certain  channels  are  easier  for  the  passing  of  this  nervous 
impulse  than  are  others.  This  is  especially  true  of  certain  reflexes  present  at  birth,  such  as 
breathing,  sucking,  etc.  Other  channels  are  made  easy  later  in  life  by  the  constant  passage  of 
impulses  along  them.  The  more  frequently  an  association  fiber  is  used  the  better  conductor 
it  becomes.  The  way  that  has  once  been  traversed  and  that  has  often  been  traversed  becomes 
the  easiest  way.  It  is  the  way  of  least  resistance  and  it  is  a  universal  rule,  whether  it  be  a 
foot-path,  or  a  conductor  of  electrical  or  of  other  force,  or  a  nerve  fiber  or  cell,  that  the  way 
of  least  resistance  is  the  easiest  way:  the  way  usually  followed.  When  not  used  for  a  long  time, 
like  a  deserted  garden  path,  the  channel  may  be  obliterated  and  the  association  lost. 

When  a  perception  occurs,  impulses  radiate  out  along  the  association  fibers  from  that  por- 
tion of  the  cortex  which  produces  it.  If  at  the  same  time  another  perception,  or  a  vivid 
memory  of  a  perception  received  a  moment  before,  takes  place  in  another  portion  of  the  cortex, 
the  association  fibers  connecting  these  two  portions  of  the  cortex,  where  perceptions  are 
occurring,  or  have  just  occurred,  being  acted  upon  at  both  ends,  will  convey  impulses  to  and 
fro  more  readily  than  the  other  association  fibers.  The  longer  and  more  frequently  the  asso- 
ciation fibers  are  traversed  by  these  impulses  the  better  conductors  do  they  become  and  these 
two  perceptions  become  more  and  more  easily  excited  the  one  from  the  other.     The  activity 

12 


in  the  cortex  does  not  long  persist;  so  that  when  the  associated  idea  is  in  consciousness,  the 
original  perception  which  awoke  it  is  already,  or  soon  will  be,  sub-conscious.  Yet  they  are 
firmly  associated  together;  so  that  whenever  in  the  future  one  enters  into  activity  it  may  excite 
the  other.  Thus,  association  between  perceptions  of  the  events  and  objects  received  simul- 
taneously, or  immediately  before  or  after  each  other,  are  formed  in  a  never-ending  stream  and 
the  events  and  objects  are  considered  as  contemporaneous  and  often  as  related  to  each  other. 
Subsequent  experiences  may  verify  and  strengthen  some  of  these  associations  and  may  disprove 
and  unmake  others.  Associations  with  any  one  perception  may  be,  and  usually  are,  extremely 
numerous.  There  is  also  an  association  of  words  as  well  as  of  perceptions,  and  the  associations 
of  words  have  no  necessary  relationship  to  the  associations  of  the  objects  which  they  represent. 
Associations  may  be  at  first  very  imperfect  and  very  difficult  to  form,  but  with  repetition  and 
practice  become  easy.  The  work  of  a  child  in  school  is  difficult  until  by  repetition  he  has 
learned  thoroughly  his  lesson.  Then  the  recitation  is  easy.  Addition,  subtraction,  etc.,  are 
at  first  performed  slowly  and  with  difficulty  but  later,  in  consequence  of  frequent  repetition, 
rapidly  and  easily. 

When  a  number  of  perceptions  are  produced  which  are  very  similar  and  yet  show  more  or 
less  individual  variations,  as  for  instance  perceptions  of  men  or  dogs,  from  a  comparison  of 
them  and  of  memories  of  others,  more  or  less  similar,  a  concept  or  idea  of  a  man  or  a  dog  is  formed, 
which  includes  all  the  individuals.  From  many  examples  of  individual  freedom  of  action,  the 
abstract  idea,  or  abstraction,  of  liberty  is  formed.  A  great  many  such  abstract  ideas  are  grad- 
ually formed  and  this  process  is  facilitated  by  the  use  of  language.  But  each  idea  is  the  result 
of  experience:  the  result  of  a  conglomeration  or  generalization  of  one  or  more  perceptions  and 
their  associations,  and,  by  the  aid  of  language,  is  given  a  name.  It  has  been  said  that  "we  can 
understand  only  so  much  of  an  abstraction  as  we  know  individual  cases  which  sustain  it." 
Thinking  and  reasoning  are  much  simplified  and  made  more  rapid  by  the  employment  of  these 
abstractions. 

Ethics 

Inasmuch  as  the  sensory  and  motor  areas  of  the  cortex  are  intimately  connected  together, 
some  perceptions  lead  to  voluntary  action,  which  may  result  in  pain,  either  directly  as  physical 
pain,  or  indirectly  as  mental  pain,  the  result  of  punishment  or  condemnation;  so  that  the  action 
and  the  perception  which  led  to  it  will  become  associated  with  these  unpleasant  sensations  or 
perceptions,  and  these  associated  unpleasant  sensations  will  tend  to  restrain  further  similar 
actions.  Such  acts,  bringing  with  them  a  penalty,  will  be  called  wrong  ami  there  will  gradually 
he  formed  a  large  number  of  associations  which  will  be  identified  with  t he  ideas  of  punishment 
and  condemnation  and  which  tend  to  prevent  the  performance  of  wrongful  nets;  just  as  another 
combination  of  associations  which  have  become  associated  with  pleasure,  reward  or  praise, 
will  be  associated  witli  good  or  right.  A  person's  idea  of  what  is  right  or  wrong  will  depend 
upon  his  education,  the  result  of  experience  and  of  teaching,  and  is  the  basis  of  emotions  ami 
ethics,  and  of  that  ill-defined  function,  the  so-called  conscience,  and  may  evolve  into  very  elab- 
orate and  very  controlling  feelings  and  habits  of  thought.  According  as  education  has  devel- 
oped one  set  of  these  associations  rather  than  the  other,  a  good  or  bad  character,  not  from  his 
own  hut  from  the  community's  standpoint,  is  formed.  These  ethical  ideas  ean  of  course  he 
imparted  from  one  person  to  another  by  language  and,  indeed,  frequently  are  so  imparled,  hut 
such  ethical  ideas  are  rarely  so  firm  and  convincing  as  those  obtained  from  experience. 

(  on.  km  u\  i  ion    \\i>   Amis  iion 
It  seems  to  be  a  general   law   in   the   physiology  of  the  nervous  system   thai    w  hen   there  is 

a  strong  activity  in  one  part,  the  activity  of  the  resl  of  the  nervous  system  is  inhibited.  Thus, 
reiiex  activity  ean  be  inhibited  by  strong  pain;  and  the  reflex  activity  of  the  spinal  cord  is  more 
or  less  inhibited  when  the  brain  is  in  activity.     In  the  brain  itself,  when  a  portion  of  the  cortex 

or  a  group  of  nerve  cell,,  fa  in  activity,  the  activity  of  the  other  cortical  areas,  as  well  a-  that 

ia 


of  the  lower  centers,  is  inhibited.  The  stronger  the  local  activity,  the  greater  and  more  exten- 
sive will  be  the  general  inhibition,  and  the  more  this  active  portion  will  have  a  free  and  unin- 
terrupted field.  Naturally,  consciousness  remains  limited  to  this  strong  activity  for  a  long 
time.  When  an  unusual  or  very  vivid  perception  or  idea  is  in  consciousness  it  occupies  the 
center  of  the  stage.  Consciousness  is  limited  to  this  one  vivid  idea  and  its  associations;  so  that 
milder  activities  occurring  in  the  cortex  at  the  same  time,  which  should  produce,  ordinarily, 
perceptions  and  associations,  remain  sub-conscious.  This  phenomenon  is  called  concentration 
and  is  a  very  important  function  in  nervous  physiology.  When  the  cause  of  this  concentration 
is  a  perception,  in  addition  to  this  inhibitory  influence,  impulses  from  the  active  sensory  cortex 
radiate  to  the  motor  cortex  and  out  to  the  perceiving  organ  and  cause  a  change  in  its  muscula- 
ture in  the  form  of  greater  tension,  tonicity,  change  in  its  position,  etc.,  which  local  change 
heightens  the  power  of  the  organ  for  the  perception  of  stimuli.  Concentration  is  only  another 
name  for  attention  and  has  been  regarded  as  an  effort,  and  an  expression,  of  the  will  or  will- 
power, but  the  primary  and  essential  factor  seems  to  be  the  cortical  activity.  (See  Will.)  Not 
infrequently  the  concentration  is  centered  about  an  unpleasant  idea,  from  the  thought  of  which 
we  vainly  try  to  escape;  yet  it  is  forced  upon  our  attention  and  we  cannot  free  ourselves  from 
it  in  spite  of  every  effort  of  our  so-called  will.  We  are  at  times  in  a  state  of  "expectant  atten- 
tion" in  regard  to  some  possible  perception,  which  state  we  cannot  prevent,  try  as  we  may. 

Reverie  and  Thought 

The  steady  stream  of  perceptions  originating  from  the  excitation  of  the  various  sensory 
organs  is  constantly  awakening  associated  memories,  and  these  memories  other  associated  mem- 
ories, and  so,  while  consciousness  remains  passive,  an  ever-varying  series  of  memories,  visions, 
day  dreams,  etc.,  flow  by.  But  consciousness  may  be  active,  and  just  as  cerebral  activities  may 
cause  either  action  or  inhibition  in  the  sub-cortical  centers,  so  the  whole  mass  and  content  of 
consciousness  may  to  a  certain  extent  strengthen  certain  memories  and  weaken  others.  This 
action  of  consciousness,  like  other  nervous  actions,  grows  stronger  by  use.  So  that  a  trained, 
educated,  intellectual  man,  is  able  to  keep  one  set  of  memories  present  in  consciousness  (atten- 
tion), to  call  up  associated  memories,  to  reject  some,  to  keep  others  active,  to  compare  them  all 
together.  This  is  called  the  act  of  thinking  or  reasoning.  The  process  of  thinking  is  thus  inde- 
pendent of  speech;  although  speech  is  essential  to  its  clear  expression  and  certainly  facilitates 
it,  especially  in  its  deep  and  profound  forms.  The  question  of  attention  is  one  which  seems  to 
require  a  more  or  less  external  will  to  keep  the  cerebral  activity  limited  to  one  subject.  Atten- 
tion is,  however,  in  part  a  manifestation  of  the  association  of  ideas.  If  many  associations  at 
the  same  time  bring  into  strong  consciousness  the  desirability  of  investigating  some  one  per- 
ception, this  idea  which  we  may  call  "a"  and  which  will  have  widespread  associations,  will 
bring  into  consciousness  this  perception  to  be  investigated,  which  we  may  call  "b"  with  its 
various  associations.  If  one  of  these  associations  leads  to  others  remote  and  unrelated,  and 
away  from  "b",  it  will  not  go  far  before  it  will  awaken  some  of  the  associations  connected  with 
"a;"  even  the  absence  of  "b"  from  consciousness  will  do  this,  and  "a"  will  be  brought  into  con- 
sciousness and  through  "a"  the  investigation  will  be  brought  back  to  "b"  again. 

When  we  have  forgotten  a  name,  we  often  cannot  by  an  effort  of  "will,"  however  strong, 
recall  it.  The  desire  for  the  name  starts  series  after  series  of  associations  in  some  way  related 
to  the  name,  which  finally  bring  it  into  consciousness.  Or  the  attempt  may  fail  and  the  desire 
may  be  unsatisfied  at  the  time.  Hours  or  days  afterwards  the  name  may  enter  consciousness 
by  some  chance  association  and  be  recognized  as  the  desired  name. 

Imagination:    Creative  Faculty 

Although  usually  one  perception  calls  up  its  associated  memories  and  keeps  repeating  them, 

in  recalling  again  and  again  past  events;  yet  unrelated  perceptions  and  ideas  may  be  present 

simultaneously,  or  nearly  so,  in  consciousness  and  may  be  artifically  associated  together  so 

that  by  such  combinations  ideas  and  scenes  may  present  themselves,  which  are  not  the  result 

14 


of  our  experience;  or  our  former  experiences  may  be  changed  or  modified  out  of  all  relation- 
ship with  themselves.  This  is  called  imagination.  It  is  the  creative  faculty  which  shows 
itself  actively  in  prose  and  poetic  works  of  the  imagination,  or  passively  in  day  dreams;  in  con- 
tradistinction to  true  facts  or  real  history. 

Consciousness  (Chart  III) 

Consciousness  consists,  at  any  instant  of  time,  of  the  then  present  perceptions  and  of  those 
past  memories  which  are  directly  or  indirectly  associated  with  these  present  perceptions  and 
which  have  been  awakened  by  them  into  activity.  Consciousness  is  thus  a  form  of  energy 
resulting  from  activity  of  the  cerebral  cortex.  The  other  memories,  not  at  that  instant  active, 
constitute  sub-consciousness  and  may  at  any  time  become  conscious  memories.  The  content 
of  consciousness  embraces  only  a  small  fraction  of  those  activities  which  take  place  in  the  brain 
and  indeed  only  a  fraction  of  those  activities  which  take  place  in  the  cerebral  cortex.  The 
activity  within  the  cerebral  cortex  must  reach  a  certain  intensity  in  order  to  produce  sufficient 
energy  to  constitute  consciousness.  When  this  cortical  activity,  although  existent,  is  less 
intense,  we  call  the  result  of  this  activity  sub-consciousness.  Such  sub-conscious  activity  may 
leave  an  ill-defined  memory  as  the  result  of  its  action.  The  conscious  and  sub-conscious  content 
of  the  brain  together  constitute  a  personality. 

A  new  born  babe  has,  probably,  no  consciousness.  An  infant  attains  consciousness  slowly 
as  he  gradually  obtains  perceptions  and  memories  and  forms  a  large  number  of  associations  of 
all  kinds.  When  an  infant  has  his  first  perception,  this  one  perception,  together  with  certain 
rudimentary  sensations  he  may  have  acquired,  constitutes  his  entire  consciousness  and  his  entire 
intelligence.  It  is  all  he  knows.  As  other  perceptions  are  obtained  and  associated  together 
his  intelligence  and  his  consciousness  become  larger,  more  distinct  and  more  complete.  The 
child  in  his  development  increases  with  great  rapidity  the  number  of  his  perceptions,  less  rapidly 
and  subject  to  many  subsequent  corrections,  that  of  his  associations,  still  less  rapidly  his  con- 
cepts, even  more  slowly  his  ethical  and  aesthetical  ideas,  and  yet  more  slowly  his  abstractions; 
but  at  the  end  of  a  tew  years  any  perception  or  memory  suggesting  action  is  subjected  to  the 
interplay  of  all  these  activities  before  the  action  is  done  or  left  undone.  In  other  words,  con- 
sciousness and  the  act  of  thinking  and  reasoning  on  which  action  is  based  (see  Voluntary  Motion) 
are  already,  even  in  childhood,  very  complicated,  perhaps  more  so  than  later  in  life,  when  action 
is  mainly  determined  by  habits  of  thought:  by  judgments  firmly  established  by  numerous 
experiences. 

Consciousness  is  a  form  of  energy  or  force,  such  as  are  light  and  electricity,  which  is  transmuted 
from  chemical  action  taking  place  in  the  cerebral  cortex.    Consciousness  embraces  nil  these  ch 
activities  which  have  "  certain  intensity;  below  this  degree  of  intensity  then  activities  constitute  .sub- 
consciousness.    The  process  is  somewhat  analogous  to  that  in  an  electric-light  hull)  through  which 

an  electric  current  inai/  be  constantly  flowing,  but  Which  only  gives  forth  light  when  the  cunt  tit  has 
attained  a  certain   intensity. 

Consciousness  is  constantly  being  newly  formed  and  is  dependent  upon  the  perceptions, 
memories,  feelings  and  ideas,  ethical  and  others,  present  at  any  one  instant.  These  phenomena 
themselves  constitute  and  are  consciousness.  None  of  them,  usually,  continues  long  in  con- 
sciousness. Others  :ire  constantly  forcing  them  out.  None  remain-  constant.  The  continuity 
of  consciousness  is  preserved  by  the  mingling  of  memories  of  past  perceptions  with  present  ones, 
and  by  memories  of  past  state-  of  consciousness. 

Consciousness  is  an  active  procest  and  depends  upon  the  integrity  and  the  blood  supply 
of  the  cerebral  cortex.    This  blood  supply  is  in  constant  ebb  and  flow  throughout  the  different 

areas  of  the  cortex;   being  at    any   instant    most    abundant    iii   those  area-  which   are  in   activity. 

Consciou  a  condition  which,  a-  yel  certainly,  we  d t  understand,  although  in  a  general 

way  we  regard  is  ai  the  result  of  chemical  changes  taking  place  within  the  cerebral  cortex.  The 
chemical  changes  themseltk  an  not  conectoueneee,  but  they  produce  this  form  of  nervous  energy 
very  much  as  a  steam  boiler  and  i  dynamo,  or  a  galvanic  battery,  produce  electricitj      W% 

Iff 


are  as  ignorant  of  the  exact  nature  of  consciousness  as  we  are  of  that  of  electricity.  These 
chemical  changes  produce  consciousness;  a  form  of  nervous  energy;  just  as  the  chemical  changes 
taking  place  in  the  muscles  produce  muscular  force;  a  form  of  mechanical  energy;  just  as  chem- 
ical changes  taking  place  in  any  living  cell  or  tissue  of  the  body  produce  a  form  of  energy  pecu- 
liar to  itself.  Consciousness  thus  locally  produced,  and  thus  continually  produced,  in  the  brain, 
passing  according  to  definite  channels  to  other  regions  of  the  cortex,  surges  through  the  brain, 
as  memories  and  ideas  are  awakened  and  cause  action  and  reaction.  The  subject  is  a  most 
difficult  one  and  is  made,  in  a  sense,  more  difficult  by  the  faculty  of  language,  which  allows  us 
to  replace  an  idea  by  a  word  of  somewhat  uncertain  definition  and  thus  leads  to  uncertain  and 
faulty  reasoning,  or  to  a  high  sounding  sentence  which  means  nothing.  Consciousness,  or 
cognition,  seems  to  be  something  added  on  to  the  essential  processes  taking  place  in  the  brain. 
The  various  association-reflexes  occurring  in  the  brain  could  take  place  and  do  take  place  quite 
as  accurately  without  consciousness,  as  for  instance  in  the  automatic  acts  of  the  somnambulist, 
or  in  the  epileptic  trance. 

The  brain  is  very  abundantly  supplied  with  blood,  especially  the  cortex,  and  the  latter 
is  very  sensitive  to  any  interference  with  its  blood  supply.  Loss  of  consciousness,  which 
occurs  normally  in  sleep  and  pathologically  in  many  conditions,  is  caused  much  more  frequently 
by  a  change  in  the  quantity  (anemia)  or  quality  (drugs  and  poisons,  including  sepsis  and  other 
autogenetic  toxic  products)  of  the  blood  supply  than  by  all  other  conditions  combined.  Per- 
versions of  consciousness,  on  the  other  hand,  seem  to  depend  less  upon  the  quantity  of  the  blood 
supply  than  upon  its  quality  (poisons)  and  upon  changes,  organic  or  functional,  in  the  cerebral 
cortex,  especially  upon  its  exhaustion. 

Personality  (Chart  III) 

Personality  is  the  sum  of  the  conscious  and  sub-conscious  content  of  the  brain.  It  expands 
as  this  content  grows  larger  and  better  systematized.  It  becomes  greater  as  during  life  a  larger 
stock  of  energy  is  accumulated  in  its  associated  memories.  It  is  stronger  as  the  consciousness 
is  more  intense  (virility).  The  "Ego"  is  the  result  of  a  long  series  of  experiences  (former  per- 
ceptions) by  which  the  body  is  differentiated  from  the  external  world  (corporeal  ego),  and  by 
which  the  complex  of  memories  and  ideas  which  the  cortex  has  accumulated  is  differentiated 
from  that  of  other  individuals  and  is  peculiar  to  itself  (mental  ego). 

The  totality  of  one's  memories  constitutes  his  experiences.  Many  similar  memories,  or 
experiences,  are  gradually  combined  into  a  general  idea  or  principle  which  becomes  a  guide,  or 
association  channel,  for  future  judgments  and  actions  and  may  persist  after  the  individual  mem- 
ories or  experiences  upon  which  it  was  founded  have  been  lost.  Cortical  excitations  of  this  nature 
are  followed  at  once  by  actions  which  are  almost  involuntary  (habits)  and  are  not  the  result 
of  a  balancing  of  many  former  memories  and  ideas  (thought).  In  this  way  one's  character 
or  personality  is  built  up.  Ideas  firmly  fixed  by  tradition,  education  and  habit,  acquire  an  over- 
whelming emotional  value.  They  not  only  exist  in  spite  of  experience  but  even  mould  experi- 
ence into  conformity  with  themselves.  Personality  is  the  result  of  the  manifold  working  of 
natural  forces.  Had  the  natural  forces  been  different  the  personality  would  have  been  different. 
Each  personality  has  its  own  history  founded  on  its  own  personal  experiences.  A  man's  per- 
sonality has  been  created  during  and  by  his  life,  in  a  brain  whose  organization  and  capacity 
have  been  modified  by  heredity. 

Personality,  being  founded  on,  and  consisting  of,  personal  experiences,  is  strongly  individual; 
but  inasmuch  as  the  large  majority  of  men  in  the  same  community  have  very  much  the  same 
experiences,  and  as  they  discuss  these  experiences  with  each  other,  there  springs  up  between 
them  a  friendly  feeling  as  beings  of  the  same  nature  and  with  the  same  interests,  needs, 
desires  and  aims.  According  to  its  education  from  its  experiences  a  personality  may  keep  itself 
apart  from  others  and  strive  only  for  its  own  well-being  and  may  thus  be  selfish  (an  egotist), 
or  it  may  merge  itself  into  the  social  life  of  the  community  and  strive  for  the  well-being  of  its 
fellow  men  as  well  as  its  own  and  thus  be  generous  (an  altruist).     In  spite  of  much  in  common, 

16 


each  personality  differs  from  others.  Some  by  their  educational  experiences  become  con  em- 
plative  men,  others  close  observers,  others  men  of  action,  etc.  Some  men  are  of  weak  char- 
acter, who  have  always  been  indulged  and  have  always  followed  the  path  of  least  resistance; 
some  are  of  strong  character,  who  have  had  to  endure  privation  and  have  learned  to  control 
their  desires.  These  different  kinds  of  men  cannot  by  any  effort  of  will  change  suddenly  their 
character,  which  has  been  formed  slowly  by  countless  past  experiences,  acting  upon  a  brain 
the  anatomical  structure  and  physiological  activity  of  which  has  been  modified  by  heredity. 
The  personality  of  a  child  has  the  potentiality  of  developing  in  the  future,  but  the  kind  of  de- 
velopment depends  more  upon  the  kind  of  future  that  is  before  it,  than  upon  its  heredity. 

Personality  seems  to  be  the  energy  resulting  from  chemical  changes  which  have  taken  place 
and  are  taking  place  in  the  cerebral  cortex  and  to  depend  absolutely  upon  the  integrity  of  the 
latter.  When  the  cortex  is  exhausted,  or  diseased,  personality  may  be  changed  under  some 
ial  experience,  resulting  from  the  undue  dominance  of  some  local  excitation  of  the  cortex, 
either  permanently  or  temporarily  (double  personality),  or  it  may  become  completely  lost 
(automatism). 

Intelligence  (Chart  III) 

Intelligence  consists  of  the  content  of  object  consciousness.  It  is  absolutely  dependent 
upon  memory,  without  which  it  cannot  exist.  The  greater  the  number  of  memories  and  the 
more  perfect  and  easier  the  recalling  of  associations,  the  greater  is  the  intelligence.  A  person's 
memories  depend  primarily  on  perceptions  derived  from  his  sensory  organs  and  on  his  experi- 
ences. The  greater  the  number  and  the  variety  of  his  experiences  the  greater  will  be  his  intel- 
other  things  being  equal.  If  any  one  sensory  organ  is  absent  or  diseased  from  birth, 
memories  of  this  sense  will  not  be  present  and  the  intelligence  will  be  diminished,  unless  this 
defect  is  in  some  way  compensated  for. 

An  increase  of  intelligence,  though  unusual,  is  not  abnormal.  In  some  cases  this  increase 
is  due  to  a  greater  number  of  perceptions  and  ideas  (the  learned  man);  in  some  cases  to  better 
and  wider  associations  throughout  the  entire  sensory  cortex  (the  wise  man),  and  in  some  cases 
one  portion  of  the  cortex  is  functionally  developed  at  the  expense  of  others  (the  genius). 

A  diminution  of  intelligence  may  be  due  to  imperfect  development,  to  impaired  nutrition 
or  to  destructive  lesions  of  the  cortex. 

Perversions  of  intelligence,  although  they  may,  in  part,  be  caused  by  peripheral  lesions, 
are  fundamentally  due  to  disease,  or  poisoning,  or  malnutrition  of  the  cerebral  cortex. 

Soul  and  Mind 
All  of  these  physiological  activities  of  the  cerebral  cortex,  which  we  have  considered  and 
which  are  popularly  called  "mental"  or  "spiritual,"  although  they  depend  upon  an  inherited 
anatomical  structure  of  the  bruin,  are  mil  preaenl  at  birth.  They  are  acquired, or  created,  during 
life  by  experience  and  by  education  in  its  broadest  sense.  They  are  the  result  of  phymologico- 
chemical  activity  within  the  cerebral  cortex.  There  is  no  scientific  or  trustworthy  evidence 
of  the  existence  of  any  further  factor  in  the  form  of  any  ethereal  essence,  a  "mind"  or  "soul" 
as  distinguished  from  what  has  been  described  above  as  "personality."  Indeed  this  assump- 
tion rather  complicates  than  simplifies  the  matter,  inasmuch  as  it  is  contradictory  to  one  of 

tin-  most   firmly  established   principles  of  natural   philosophy:  "the  law  of  th mservat  ion  of 

energy."     This  law  has  not   only  been  established   by  irrefutable  proof  in  the  inorganic  world, 
but  also  has  been  proved  by  experiment   to  be  valid  in  animals  and  even  in  man.      If  (' 

can  produce  or  stop  a  cerebral  activity  of  its  own  volition,  thus  ci  mnihilating  force 

which  normally    proceeds    in    an  endless  chain  from  one  manifestation  of  force  to  another,  then 
the  law  of  the  conservation  of  energy  is  no  longer  valid. 

Mankind  has  been  unwilling  to  allow  that  the  causalities  and  laws,  which  prevail  in  physi- 
cal activities,  can  he  potenl  also  in  the  body  and  still  less  in  the  brain  and  "mind,"  because 

this  controverts  all  their  preconceived  notions  of  the  soul  and    its    relation  to  God.      The  preju- 
pre-judgments)  of  mOSl   men  will  not   permit   them  to  regard  the  mental  activities  as  the 

17 


result  of  the  physiological  activity  of  the  cerebral  cortex,  in  the  same  way  that  the  physiological 
activities  of  the  other  internal  organs  of  the  body  produce  and  cause  the  functions  of  these 
organs.  They  are  unwilling  to  regard  psychology  as  identical  with  the  physiology  of  the  cere- 
bral cortex.  In  earlier  historic  times,  the  winds  from  the  cardinal  points  of  the  compass, 
rippling  streams,  cascades,  the  waves  of  the  sea,  growing  trees  and  shrubs,  etc.,  were  each  sup- 
posed to  be  animated  by  an  indwelling  spirit.  At  the  present  time,  Naiads,  Nereids,  Dryads 
and  other  Nymphs:  charming  creatures  of  the  imagination,  have  all  been  banished  by  the  advance 
of  knowledge.     Only  the  indwelling,  animating  spirit  of  man:  the  soul,  remains. 

Whether  an  individual  believes  in  a  soul  or  not,  depends  upon  his  traditions,  his  education, 
his  experiences  and  upon  the  personality  which  has  been  gradually  created  and  developed  during 
his  lifetime  by  the  combination  of  all  those  forces  constituting  consciousness  and  sub-conscious- 
ness, and  which  may,  in  a  sense,  be  likened  to  the  older  conception  of  a  soul.  It  seems  probable 
that  consciousness,  intelligence,  personality,  etc.,  are  forms  of  energy  and  force  and  may,  per- 
haps, be  called  spiritual  in  contradistinction  to  material.  Whether  this  energy  or  force,  which 
is  gradually  accumulated  during  life,  persists  after  death,  we  do  not  know.  It  certainly  is  abso- 
lutely dependent  upon  the  blood  supply  of  the  cortex,  and  when  this  is  arrested,  personality  with 
every  other  manifestation  of  consciousness  ceases;  but  it  still  exists  potentially  and  may  be 
reanimated,  if  the  circulation  be  restored  after  an  interval  of  only  a  few  minutes.  If,  however, 
the  arrest  of  the  circulation  is  so  long  that  the  cortex  begins  to  degenerate  or  die,  the  personality 
is  lost  permanently,  both  actively  and  potentially. 

Our  knowledge  in  comparison  with  the  wonders  of  the  Universe  is  infinitely  small.  We  know 
the  relation  of  things,  not  their  essence.  But  our  knowledge  is  increasing  and  it  is  to  be  hoped 
that  our  children's  children  may  have  a  higher  point  of  view  and  a  clearer  vision. 

Insanity  (Charts  III  and  XVI) 

Whether  we  believe  in  the  existence  of  a  soul  within  the  body  or  not,  certainly  insanity 
is  no  longer  regarded  as  the  possession  of  the  body  by  an  evil  spirit  (demoniacal  possession). 
This  was  a  well  established  belief  for  ages,  but  it  has  long  since  been  abandoned  and  we  now  re- 
gard insanity  as  caused  by  abnormal  cerebral  action.  The  control  of  the  body  by  a  spirit, 
which  we  have  finally  rejected  as  regards  insanity,  the  vast  majority  of  mankind  still  retains 
for  the  healthy  body,  possibly  because  most  of  the  few  men  who  really  think  have  not  studied 
cerebral  physiology. 

We  have  considered  briefly  the  actions  taking  place  in  the  sensory  area  of  the  normal, 
healthy,  cerebral  cortex.  In  an  abnormal  cortex  these  actions  are  deranged.  Local  disordered 
cortical  function  produces  local  paralysis  or  apraxia  or  convulsions  or  even  hallucinations; 
while  general  disordered  function  produces  coma,  neurasthenia,  or  insanity.  Abnormal  struc- 
ture, whether  the  alteration  be  slight  or  great,  and  consequently  abnormal  function,  of  the 
cerebral  cortex  may  be  either  congenital  or  acquired.  The  congenital  form  may  be  manifest 
in  early  infancy  or  may  become  apparent  at  any  stage  of  the  individual's  development,  as  he 
successively  meets  tasks  which  require  more  and  more  intellectual  power,  when  it  becomes 
evident  that  his  intelligence  and  ethics  fall  below  the  commonly  accepted  standards  of  the  race 
or  community  of  which  he  is  a  member. 

The  greatest  degree  of  absence  of  intelligence  is  idiocy  (1081),  which  shows  itself  almost  at 
birth.  In  this  disease  the  brain  is  so  functionally  incapable  that  it  cannot  produce  perceptions,  or 
register  memories,  or  form  associations,  except  of  the  most  rudimentary  kind.  These  persons, 
then,  have  no  material  for  intelligence,  consciousness  or  ethics  and  are  incapable  of  speech. 
Next  to  this  extreme  degree  is  imbecility  (1088),  which  may  show  itself  at  any  time  from  birth  to 
early  childhood.  In  this  class,  simple  perceptions,  memories,  associations  and  speech  are  possible, 
but  only  very  imperfectly,  and  there  is  very  limited  material  for  consciousness,  intelligence  or 
ethics.  A  still  slighter  degree  of  this  condition  is  only  manifested  when  a  considerable  degree 
of  intelligence  or  ethics  is  imperatively  required,  especially  at  the  so-called  critical  periods  of 
life,  as  at  puberty  (some  forms  of  adolescent  insanity — 1096).     Although  individuals  of  this 

18 


class  have  memories,  associations  and  consciousness,  their  intelligence,  ethics  and  judgment 
are  found  to  be  inferior  to  those  of  their  fellows  educated  under  the  same  conditions  and  they 
are  called  feeble-minded  and  defectives  (1092)  in  varying  degree.  In  the  slighter  forms  of  this 
class  only  the  higher  and  more  complicated  ideas,  such  as  altruism  and  morality,  are  absent 
or  impaired  (moral  insanity  and  some  criminals).  In  the  severer  forms,  the  loss  is  more  profound 
and  involves  all  the  cortical  functions. 

In  other  cases  of  congenitally  defective  brain  the  defect  is  very  slight,  but  some  of  the  asso- 
ciation channels  are  more  patent  than  others,  and  than  is  normal;  so  that  certain  associations 
and  ideas  are  constantly  being  presented  to  consciousness  and  are  called  up  by  all  kinds  of  un- 
related associations  and  cannot  be  corrected,  and  consequently  the  cortical  actions  are  distorted 
and  twisted  and  irrational.     To  this  class  belong  the  paranoides  (1113). 

Education  and  training  have  much  to  do  with  the  development  of  the  activity  of  the  cere- 
bral cortex  and  consequently  with  the  individual's  intelligence  and  ethics.  There  are  individ- 
uals who,  partly  in  consequence  of  a  defective  brain,  but  mainly  in  consequence  of?a  defective 
training  and  education,  do  not  have  normal  experiences  and  form  a  number  of  abnormal  asso- 
ciations and  ideas,  especially  ethical.  Such  individuals  comprise  the  majority  of  criminals 
and  cranks.  Such  cases  bridge  over  the  separation  between  the  congenital  and  the  acquired 
forms  of  insanity.  Of  course,  it  is  possible  that  a  person  with  a  normal  brain,  who  is  isolated 
from  his  fellow  beings  and  receives  no  training  or  education,  will  be  feeble-minded  or  even  an 
imbecile. 

All  these  congenital  forms  of  insanity  may  be  broadly  classed  under  the  term  amentia  (211, 
1076)  in  its  widest  sense:  the  mind  never  having  fully  developed.  On  the  other  hand  all  the 
acquired  forms  of  insanity  may  be  broadly  classed  under  the  term  dementia  (212,  1077)  in  its 
widest  sense:  since  there  is  always  present  a  certain  mental  weakness  not  previously  present, 
a  falling  off  in  greater  or  lesser  degree  from  the  previous  more  perfect  cortical  activity. 

Acquired,  disordered  activity  of  the  cerebral  cortex  resulting  in  insanity  primarily  also 
depends  upon  a  defective  brain,  either  hereditary  or  acquired,  but  secondarily  upon  many  in- 
citing causes.  It  may  be  due  to  a  general  deficiency  in  the  blood  supply  consequent  upon  athero- 
matous arteries,  as  in  senile  dementia  (1105);  or  may  be  due  to  an  irregular  cortical  circulation 
consequent  upon  chronic  meningitis;  the  most  striking  example  of  this  class  being  paresis  (1  Id!  i. 
Various  poisons  (alcohol,  etc.),  endogenous  or  exogenous,  are  responsible  for  other  forms  of 
insanity  which  are  usually,  but  not  always,  of  comparatively  short  duration.  Local  lesions  of  the 
brain,  surh  as  abscess,  tumors,  etc.,  may  in  some  cases  alter  the  circulation  of  blood  through  the 
cortex  generally  and  thus  cause  insanity.  Exhaustion  of  the  cerebral  cortex  from  worry,  anxiety, 
shock  and  other  causes  may  cause  insanity  in  persons  with  an  unstable  brain,  as  may  also  an 
anemic  and  altered  condition  of  the  blood.  It  is,  of  course,  possible  that  several  of  the  above 
causes  act  simultaneously,  or  in  sequence,  and  as  a  matter  of  fact  they  frequently  do  so. 

In  most  of  the  forms  of  insanity  the  altered  cortical  activity  manifests  itself  in  certain 
striking  and  unusual  phenomena.  One  of  these  is  hallucinations  (2i:>,  L078),  which  are  abnormal 
perceptions.      In  hallucinations  the  symbol  occurring  in  the  cortex  does  not  correspond  to  any 

external  phenomenon,  bul  is  purely  subjective,  and  is  due  to  disturbances  in  the  cortex  itself, 

not  in  the  peripheral  sense  organs.  The  hallucinations  may  occur  in  any  of  the  special  sensory 
regions  of  the  cortex  and  hence  may  be  either  olfactory,  gustatory,  visual,  auditory,  tactile,  or 
even  visceral.     The  process  in  the  brain  which  produces  an  hallucination  must  he  similar  to  that 

which  produces  a  perception.    An  hallucination  is  much  more  vivid  than  a  memory  and  an 

hallucination  is  not  a  complete  and  correct  reproduction  of  a  former  memory,  but  usually  is 
Something  strange  and  hi/.arre.      In  some  cases  the  hallucinal  ions  do  not   have  tin-  vivido 

true  perceptions,  bu1  seem  to  lie  internal  voices  of  suggestions,  telephonic  communications  or 

electrical    action,    etc. 

An  illusion  i  .1  |i   i-  also  a  false  perception,  but   it  originates  from  an  external  reality  which 

is  misinterpreted  in  the  brain:  the  symbol  in  the  cerebral  cortex  is  not  such  as  is  usual]} 
dated  by  the  average  man  with  the  external  object,  hut  rather  a  symbol  usually  associated 

19 


with  a  quite  different  object.  Hallucinations  and  illusions  may  occur  as  the  result  of  a  local 
disturbance  in  a  brain  which  may  not  be  for  the  moment  entirely  normal,  although  the  individual 
is  certainly  not  insane.  In  such  cases,  hallucinations  and  illusions  can  be  quickly  dispelled  by 
reason  and  by  proof  of  their  abnormal  character.  Insane  persons,  however,  in  consequence 
of  a  diffuse  cortical  disturbance,  cling  to  their  hallucinations  and  illusions  with  great  tenacity 
in  spite  of  strong  proof  to  the  contrary.  These  hallucinations  and  illusions  occurring  in  a  brain 
weakened  by  nature,  poison  or  disease,  naturally  lead  to  abnormal  associations  and  consequently 
to  abnormal  ideas.  Abnormal  associations  will  result  not  only  from  the  strength  and  vividness 
of  these  hallucinations,  but  also  because  from  patches  of  meningitis,  or  other  cause,  some  areas 
of  the  cortex  have  more  blood  than  others  and,  therefore,  respond  more  readily  to  association 
impulses,  near  and  remote.  Moreover  these  abnormal  ideas  entering  into  consciousness  and 
coming  into  conflict  with  former  long  established  ideas  lead  to  a  condition  of  consciousness  which 
we  call  bewilderment,  clouded,  befogged,  confusion,  distrust,  apprehension,  fear,  etc.  In 
these  cases,  impulses  reaching  the  cortex  normally  from  the  organs  of  sense  are  so  much  weaker 
than  the  excitations  already  there,  that  they  cannot  enter  into  consciousness,  but  remain  sub- 
conscious. They  may,  although  sub-conscious,  be  registered  and  may  be  recalled  to  conscious- 
ness after  the  attack  of  insanity  is  past,  but  they  have  no  present  value  and  are  inadequate  to 
correct  the  abnormal  activities  and  no  sane  judgment  can  result. 

A  cortex  in  which  normal  perceptions  can  occur  only  imperfectly,  or  not  at  all,  and  in  which 
abnormal  perceptions,  associations  and  ideas  are  dominant,  will  naturally  produce  abnormal 
association  reflexes,  or  actions.  The  simplest  of  these  is  delirium  (217,  1107-8),  in  which  the 
patient  responds  by  word  and  act  to  the  many  false  perceptions  and  ideas  in  his  clouded  and 
weakened  consciousness.  When  the  intensity  of  the  process  is  less  the  false  perceptions  and 
ideas  will  produce  delusions  (215,  1079),  which  will  cause  abnormal  and  often  dangerous  asso- 
ciation reflexes  or  acts.  These  delusions  may  remain  isolated,  unsystematized  or  may  be  woven 
in  with  all  the  real  experiences  of  the  individual  life;  so  that  a  systematized  delusion,  founded 
upon  more  or  less  evidence  or  reasoning,  acting  upon  a  weakened  or  limited  general  cortical  activity 
or  judgment,  results. 

Often  in  justifying  or  explaining  a  delusion  a  patient  will  give  reasons  or  cite  experiences 
which  we  call  false,  but  which  are  doubtless  experiences,  the  symbols  of  which  have  occurred 
in  his  abnormally  acting  cerebral  cortex.  These  delusions,  or  false  and  uncorrectable  judgments, 
naturally  lead  to  acts  which  are  incompatible  with  an  unconstrained  life  in  a  reasonable  com- 
munity. Naturally  with  all  these  abnormal  cortical  activities  not  only  the  ethical  ideas  of  the 
individual  are  changed,  but  also  the  normal  emotions  associated  with  normal  cortical  activity 
are  profoundly  altered,  whether  in  the  form  of  exaltation  or  depression,  either  continuously  or 
in  alternation  with  each  other. 

In  all  forms  of  insanity,  in  consequence  of  its  abnormal  content,  consciousness  is  altered 
and  personality  may  be  changed.  There  may  be  a  double  personality  or  the  individual  may 
imagine  that  he  is  dead,  an  animal,  a  king,  or  God,  or,  in  extreme  degrees  of  dementia,  the 
patient  may  show  no  consciousness  or  personality  at  all.  The  emotions  are  also  altered  (morbid 
temperaments)  in  accordance  with  the  ideas  in  consciousness,  or  may  be  entirely  dissociated 
from  the  ideas  with  which  they  are  normally  in  harmony,  or  may  be  entirely  absent  in  extreme 
dementia,  or  may  be  feebly  carried  over  from  former  highly  emotional  states.  The  emotion 
most  frequently  present,  especially  in  the  early  stages  of  the  disease  is  fear  (phobias). 

Fear  and  apprehension  are  prominent,  even  dominant,  symptoms  in  the  early  stages  of 
almost  every  case  of  insanity.  The  unusual,  often  monstrous,  phenomena  occurring  in  the 
cerebral  cortex  are  so  different  from  those  previously  present  and  so  out  of  harmony  with  former 
memories  and  ideas,  that  the  patients  naturally  become  distrustful,  apprehensive  and  full  of 
fear.  Many  can  hardly  believe  the  information  supplied  by  their  own  senses,  much  less  the 
words  of  their  friends.  Some  regard  themselves  as  persecuted  and  as  the  victims  of  conspira- 
cies.    Fear  is  the  dominant  emotion  within  them. 

20 


The  association  reflexes  are  always  altered  in  insanity  in  consequence  of  the  abnormal 
cortical  activity.  In  extreme  dementia,  voluntary  motion  is  completely  abolished.  In  pro- 
found melancholia,  voluntary  acts,  as  well  as  thought,  are  inhibited;  while  the  reverse  is  true 
in  mania,  in  which  cortical  activity,  although  abnormal,  is  greatly  exaggerated.  In  consequence 
of  prominent,  compulsory  ideas,  so  frequent  in  insanity,  compulsory  acts  result. 

Movement  (Charts  IV  and  V) 

When  a  sensory  surface  is  irritated  the  animal  often  responds  immediately  by  a  compara- 
tively simple  movement,  or  the  movement  may  occur  only  after  a  considerable  space  of  time 
and  may  be  very  complicated,  or  it  may  never  occur.  Movements  may  also  occur  spontane- 
ously, apparently  not  being  preceded  by  any  sensory  irritation  in  the  immediate  past;  although 
on  careful  analysis  these  spontaneous  movements  can  always  be  referred  back,  indirectly,  to 
some  sensory  irritation.  All  these  different  kinds  of  movements  are  divided  into  three  great 
classes:  reflex,  voluntary  and  automatic. 

Reflex  Action  and  Inhibition  (Chart  V) 

A  reflex  act  is  a  reaction  from  an  irritation,  which  under  like  conditions  always  takes  place 
in  exactly  the  same  way;  it  seems  purely  mechanical,  as  if  a  machine  were  working.  The  irri- 
tation may  be  a  usual  (normal  or  adequate),  or  an  unusual  (abnormal  or  inadequate),  one;  the 
former  being  much  more  effective,  and  it  may  affect  the  skin,  mucous  membrane,  or  muscle, 
tendon  or  fascia,  or  any  of  the  organs  of  special  sense.  The  impulse  starts  in  the  end-organ 
of  a  sensory  nerve  supplied  to  the  sensory  organ  affected  and  passes  centripetally  along  the 
peripheral  sensory  nerve  fiber,  or  fibers,  to  the  spinal  or  cranial  ganglion,  situated  on  the  pos- 
terior spinal,  or  the  cranial,  nerve  root.  Thence  it  passes  forward  through  the  posterior  horn 
to  the  anterior  horn  of  the  spinal  cord,  or  through  the  brain  stem  to  a  cranial  motor  nucleus, 
and  thence  along  a  motor  nerve  root  and  peripheral  nerve  to  a  muscle  or  muscles,  striated  or 
unstriated,  in  which  it  causes  a  contraction,  or  to  a  gland  in  which  it  causes  an  alteration  in 
its  secretion  (Fig.  24).     Muscular  tonicity  is  a  variety  of  reflex  action  (240). 

The  various  nervous  elements  traversed  by  the  nervous  impulses,  as  just  described,  con- 
stitute what  is  called  "the  reflex  arc"  (296).  Slight  irritative  lesions  of  the  reflex  arc  cause 
exaggeration,  while  destructive  lesions  cause  abolition,  of  reflex  action.  This  is  the  simplest 
form  of  nervous  reaction  and  this  is  the  simplest  expression  of  it.  Such  simple  reflex  acts  are 
the  only  ones  occurring  in  the  body  during  the  early  months  of  life  and  are  unconscious  acts. 
Similar  reflex  acts  cause  the  respiratory  and  cardiac  movements,  the  Bow  of  saliva  and  other 
secretions,  the  vascularity  of  organs  and  the  warmth  of  the  body,  and  in  general  regulate  the 
physiological  actions  of  the  body. 

When  the  nervous  impulse  reaches  the  gray  matter  of  the  central  nervous  organs  so  many 

ways  of  transmission  are  open  to  it  that  it  can  pass  by  longer  or  shorter  arcs  or  by  several 
of  them.  The  shortest  possible  reflex  arc  is  through  a  peripheral  ganglion  (as  in  the  vaso- 
motor reflexes).    The  next  shortest  is  through  the  spina]  cord.    A  longer  one  is  through  the 

spinal    cord    and    the   ganglia    at    the    base   of   the    brain.      The   longest    is    through    the   cerebral 

cortex.    Some  reflex  acts,  such  as  the  pupillary  (302),  remain  unconscious  acta  throughout 

life.  On  the  other  hand,  most  of  the  sensory  impulses  described  al>ove,  when  they  have  tra- 
versed the  sensory  nerves  and  have  reached  the  senary  ganglia,  pass  in  part  as  described  above 
to  the  motor  nuclei,  but  pan  also  in  part  up  the  central  sensory  conducting  tracts  to  the  higher 
ganglia  :,1  the  base  of  the  brain;  where  they  may  cause  more  complicated  reflex  acts  and  pass 
still  higher  to  the  sensory  cerebral  cortex;  where  they  may  give  rise  to  sensations  and  percep- 
tions (Fig.  36).  Here  the  impulses  may  apparently  stop,  or  they  may  be  continued  from  the 
BenBOiy  OOrteX  tO  the  motor  cortex  and  thence  a  new  impulse  may  pan  downward  along  the 
pyramidal  tract,  and  thus  the  involuntary  reflex  act  may  be  increased  or  replaced  by  a  volun- 
tary   act,  or  may   be  abolished   (inhibited),   voluntarily. 

■J  I 


This  voluntary  abolition  of  reflex  activity  (inhibition)  may  be  brought  about  by  a  contrac- 
tion of  those  muscles  which  antagonize  the  muscles  taking  part  in  the  reflex  act,  or  this  latter 
act  may  be  "inhibited"  by  a  direct  action  upon  the  sub-cortical  motor  cells  taking  part  in  it. 
In  addition  to  this  voluntary  inhibition,  a  great  variety  of  nervous  activities  taking  place  in 
almost  any  part  of  the  nervous  system  (especially  strong,  painful  impressions),  and  even  the 
normal  process  of  cerebral  activity,  will  cause  a  more  or  less  complete  inhibition  of  reflex  activity. 
It  seems  as  though  two  impulses  acting  upon  a  cell  at  the  same  time  under  certain  conditions 
may  mutually  counteract  each  other.  Therefore,  reflex  activity  is  more  active  in  animals  in 
which  the  brain  (or  even  other  parts  of  the  nervous  system)  is  separated  from  the  spinal  cord 
or  reflex  centers  and  in  human  beings  when  the  same  result  is  accomplished  by  disease  (isola- 
tion). Curiously  enough,  when  the  human  spinal  cord  in  its  upper  part  is  completely  destroyed 
the  reflex  activity  of  the  lower  parts  of  the  cord  is  abolished.  This  phenomenon  has  not  been 
satisfactorily  explained  and  is  in  marked  contrast  to  the  exaggerated  reflexes  found  in  incom- 
pletely destructive  lesion  of  the  upper  portion  of  the  cord. 

Conduction  of  reflex  or  other  impulses  along  the  peripheral  nerves  is  equally  rapid  what- 
ever may  be  the  intensity,  or  quality,  of  the  irritation,  but  conduction  through  the  gray  matter 
is  much  slower  and  varies  greatly  with  the  intensity  and  quality  of  the  irritation.  The  gray 
matter  also  possesses  the  power  of  summation;  so  that  inactive  excitations  may  become  active 
ones  by  repetition.  The  gray  matter  immediately  following  its  activity  shows  a  "refractory 
period"  of  longer  or  shorter  time  during  which  is  it  inexcitable  or  exhausted.  This  indicates 
that  the  gray  matter  accumulates  energy  during  rest,  which  it  discharges  when  in  activity. 
This  refractory  period  may  play  its  part  in  rhythmical  action.  Most  reflex  acts  are  purposeful 
and  healthful  in  their  nature.  Many  of  them  are  absolutely  essential  for  life.  They  may  be 
divided  into  the  offensive  and  the  defensive. 

A  destructive  lesion  of  any  portion  of  the  reflex  arc  causes  abolition  of  the  reflex  acts,  as 
does  also  a  strong  irritation  of  the  higher  nervous  centers.  Slight  irritative  lesions,  such  as 
slight  inflammations,  will  cause  an  exaggeration  of  the  reflex  act,  as  will  also  and  more  commonly 
a  lesion  which  interferes  with  conduction  of  nerve  impulses  (inhibitory  impulses)  through  the 
central  motor  (or  cortico-spinal)  neurons.  An  irritation,  especially  a  continuous  one,  even  if 
not  very  intense,  will  often  cause  a  tonic  spasm  or  contracture. 

Voluntary  Action,  Association  Reflexes  (Chart  IV) 

The  anterior  portion  of  the  cerebral  cortex,  which  contains  innervation  (kinesthetic) 
memories,  or  motor  centers,  is  connected  through  bundles  of  association  fibers  with  the  pos- 
terior portion  of  the  cortex,  in  which  are  memories  obtained  from  the  organs  of  sense.  Activity 
never  normally  originates  directly,  or  spontaneously,  in  the  motor  cortex,  but  comes  to  it  from 
the  sensory  cortex.  When  a  very  strong  excitation  arises  in  this  sensory  cortex,  as  for  instance 
perceptions  which  are  associated  with  the  idea  of  imminent  danger  of  death,  this  excitation 
passes  to  the  motor  cortex  and  thence  down  through  the  internal  capsule  and  pyramidal  tract 
and  causes  movements  of  flight  and  self-preservation.  This  act  is  as  inevitable  and  as  machine- 
like as  is  the  simplest  reflex  act.  A  good  swimmer  bent  on  suicide  cannot  drown  himself  unless 
he  is  weighted  or  the  action  of  his  knees  or  legs  is  restricted.  Escape  from  imminent  death  is 
for  most  men  an  imperative  voluntary  act.  If,  however,  the  danger  is  less  great,  as  on  a  battle- 
field, the  excitation  leading  to  flight  may  be  still  there,  but  it  may  be  inhibited  by  excitation 
from  other  associations,  such  as  the  idea  of  shame,  love  of  country,  etc.,  and  the  two  excitations 
may  neutralize  each  other.  It  is  a  question  which  idea:  the  fear  of  death  or  the  love  of  country 
and  honor,  is  based  on  stronger  perceptions  and  wider  and  stronger  associations.  Whichever 
is  the  stronger  prevails. 

Ordinarily,  when  a  perception,  or  memory,  suggesting  action  has  sufficient  intensity  to 
enter  consciousness,  the  excitation  is  sufficiently  strong  to  pass  along  the  association  fibers  and 
awaken  into  activity  the  corresponding  innervation  memories  and,  if  no  other  counteracting 
excitation  comes  to  this  latter  portion  of  the  cortex,  the  irritation  passes  through  the  great 

22 


motor  cells  in  the  anterior  central  convolution  and  down  through  the  internal  capsule  and  pyra- 
midal tract  and  the  action  takes  place.  Actions  resulting  from  memories  are  usually  weaker 
than  those  resulting  from  the  original  excitation  or  perception.  When  a  number  of  more  or 
less  conflicting  memories  and  ideas  are  in  consciousness,  some  for  and  some  against  the  action, 
impulses  will  be  constantly  coming  to  the  motor  cortex  to  be  either  immediately  inhibited,  or 
strengthened.  The  play  of  the  different  perceptions,  memories  and  ideas:  the  play  of  motives, 
may  continue  a  long  time  as  the  person  deliberates  and  exercises  his  free-will.  This  merely  means 
that  the  different  memories,  together  with  the  ideas  derived  from  the  mass  of  associated  mem- 
ories which  constitute  our  ethics  and  those  which  constitute  our  emotions,  have  sufficient  in- 
tensity to  act  upon  the  motor  cortex,  some  as  excitants,  some  as  inhibitors.  Fresh,  allied  mem- 
ories constantly  enter  consciousness,  because  of  their  association  with  those  already  in  it,  and 
take  part  in  this  phenomenon.  It  is  like  a  debating  society  in  which  arguments  for  and  against 
are  presented  almost  simultaneously,  and  the  stronger  argument  rather  than  the  will  of  the 
judge  is  the  decisive  factor.  It  is  probable  also  that  sub-conscious  activities  may  play  some 
part  in  this  process.  Eventually  the  stronger  excitation  will  prevail  and  the  act  will  be  either 
done  or  left  undone. 

A  voluntary  act,  depending  upon,  and  being  the  result  of,  the  association  of  ideas,  may  be 
described  as  an  association  reflex.  The  idea  of  the  apparent  freedom  of  will  depends  upon  the 
absence  of  external  compulsion  and  also  upon  the  fact  that  the  action  takes  place,  or  does  not  take 
place,  in  accordance  with  the  relative  strength  of  our  ideas  and  desires.  The  more  perceptions 
and  ideas  a  person  has  in  his  memory,  the  more  learned  and  intelligent  he  is,  the  greater,  wider 
and  more  protracted  will  be  this  "play  of  motives"  and  the  more  difficult  will  be  the  choice  of 
the  resulting  action:  the  association  reflex,  the  victory  of  any  one  set  of  motives.  The  very 
learned  man  is  not  the  man  of  action.  In  a  child  or  in  an  ignorant  man,  with  tewer  elements 
of  a  choice,  the  association  reflex  may  be  more  prompt.  When  a  decision  under  the  same  or 
similar  conditions  is  made  a  second  time,  and  especially  when  frequently  repeated,  the  asso- 
ciation reflex  takes  place  more  and  more  promptly.  In  the  frequent  repetition  of  acts:  prac- 
tice, the  same  association  conducting  channels  are  being  constantly  traversed  and  consequently 
become  better  conductors,  and  the  acts  become  easier  to  perform:  become  more  or  less  auto- 
matic. It  becomes  a  habit.  A  large  part  of  our  voluntary  acts  are  habitual.  It  is  to  be  remem- 
bered also  that  the  internal  sensations,  which  dominate  our  "moods,"  exercise  a  strong  influence 
over  voluntary  movements  which,  under  changing  moods  and  altered  internal  sensations  may 
be  very  different  at  different  times,  although  the  causal  external  sensation  is  the  same. 

The  gray  matter:  the  point  of  union  of  the  motor  and  sensory  neurons,  is  in  small  com- 
pass in  the  sub-cortical  centers  and  hence  is  well  fitted  for  direct  transference  for  reflex  and 
automatic  actions.  In  the  cortical  centers  the  gray  matter  is  spread  over  a  large  surface  and 
permits  separate,  local  action,  and  consequently  permits  a  large  number  of  different  memories 
and  ideas,  some  positive  and  some  negative,  to  act  simultaneously  upon  the  motor  cortex  and 
thus  either  cause  or  prevent  a  voluntary  action.  Both  voluntary  and  reflex  acts  are  for  the 
benefit  of  the  individual.  The  reflex  acts  depend  upon  heredity  and  evolution.  They  are  the 
result  of  the  experiences  of  the  individual's  ancestors,  of  the  experience  of  the  race  (phylo- 
genetic).  Voluntary  acts  depend  upon  the  individual's  personal  experience  (ontogenetic).  The 
difference  between  the  two  depends  mainly  on  differences  in  anatomical  structure.  In  con- 
ditions which  are  new  and  in  which  no  experience  can  guide  him,  an  individual's  voluntary  acts 
are  quite  as  likely  to  be  detrimental  as  salutary.  His  reflex  acts  almost  without  exception  are 
salutary. 

The  innervation  memories  stored  in  the  motor  cerebral  cortex  are  originally  acquired  from 
reflex  acts.  The  firM  voluntary  acts  of  the  child  (BUCking,  opening  ami  closing  eyes,  closing  of 
hand,  etc.)  are  adopted  reflex  acts,  either  unmodified  or  but  slightly  modified.  A  young  infant 
doei  not  will  (o  suck  milk  from  his  mother's  bre.i-i  |i  \  a  reflex  act.  Hut  after  the  infant 
perienoed  the  result  of  this  act  B  lufficianl  number  of  times,  the  sight  of  oil  mother,  or 
hunger,  may  awaken  his  desire  and  he  will  suck  the  breafll   voluntarily  in  consequence  of  this 

23 


active  memory.  Voluntary  motions,  or  association  reflexes,  occur  early  and  develop  rapidly  in 
infantile  life,  but  occur  much  earlier,  though  the}'  develop  much  slower,  in  young  animals. 
Chickens  run  almost  as  soon  as  they  are  born  to  their  mother  when  she  "clucks"  for  them. 
The  lower  animals  thus  possess  at  birth,  by  heredity,  a  more  perfect  nervous  system;  while 
human  infants  possess  at  birth  by  heredity,  one  less  perfect,  but  capable  of  a  wonderful  develop- 
ment, which  results  in  greater  part  from  personal  experiences. 

A  normal  voluntary  motion  depends  not  only  upon  a  fairly  healthy  cerebral  cortex  (which 
implies  a  certain  degree  of  intelligence)  and  a  normal  muscle,  but  also  upon  the  integrity  of  the 
two  motor  neurons:  the  central  (corticospinal)  and  peripheral  (spino-neural) ,  or  the  upper  and 
lower  (461-2).  The  impulse  causing  the  voluntary  contraction  starts  (as  regards  its  purely 
motor  function)  in  the  cell  body  of  the  central  motor  neuron  lying  in  the  anterior  central  con- 
volution (Fig.  15).  It  passes  along  the  axon  of  the  cell,  which  becomes  the  axis  cylinder  of  a 
nerve  fiber,  through  the  corona  radiata,  the  anterior  portion  of  the  posterior  limb  of  the  internal 
capsule  (Fig.  17),  and  emerges  from  the  cerebral  hemisphere  at  the  base  of  the  brain  in  the  pes 
cerebri.  It  is  then  covered  by  the  transverse  fibers  of  the  pons  Varolii,  from  the  lower  edge  of 
which  it  emerges  to  help  form  the  anterior  pyramids  of  the  medulla  oblongata  (Figs.  20-22). 
At  the  junction  of  the  medulla  with  the  spinal  cord,  these  fibers  of  the  anterior  pyramids  in 
great  part  decussate;  the  completeness  of  this  decussation  varying  somewhat  in  different  indi- 
viduals (Fig.  23).  Usually  the  great  majority  of  the  fibers  decussate  and  run  down  through  the 
spinal  cord  in  the  posterior  part  of  the  lateral  column  (crossed  pyramidal  tract),  a  small  minority 
of  the  fibers  running  down  in  the  anterior  column  of  the  same  side  as  the  pyramid  and  close  to 
the  anterior  median  fissure  (direct  pyramidal  tract)  (Fig.  26).  In  certain  extremely  rare  cases 
no  decussation  takes  place.  The  fibers  from  both  the  direct  and  the  crossed  pyramidal  tracts 
pass  to  the  groups  of  motor  nerve  cells  lying  in  the  anterior  horns  (Fig.  26),  and  to  these  cells 
they  communicate  their  impulses.  (The  course  of  these  central  motor  neurons  is  shown  in  Fig. 
34.)  From  the  group  of  nerve  cells  in  the  anterior  horns  of  the  spinal  cord,  these  impulses, 
thus  communicated,  pass  out  along  the  axons  of  the  cells,  which  axons  become  the  axis  cylinders 
of  the  anterior  nerve  roots,  and  thus  pass  along  the  peripheral  motor  nerve  fibers  to  the  group 
of  muscles  innervated  by  this  group  of  nerve  cells  in  the  anterior  horn.  These  impulses  enter 
the  muscles  by  the  motor  end  plates  and  cause  a  muscular  contraction. 

Although  the  cortical  motor  centers  represent  almost  exclusively  muscles  lying  on  the 
opposite  side  of  the  body,  it  appears  from  clinical  observation  and  physiological  experiment 
that  the  muscles  of  the  body  have  a  bilateral  cortical  representation.  By  electrical  stimulation 
of  the  cortex  the  muscles  on  the  same  side  of  the  body  may  be  made  to  contract,  although  a 
much  stronger  irritation  of  the  center  is  needed  than  is  necessary  to  cause  a  contraction  of  the 
corresponding  muscles  on  the  opposite  side  of  the  body.  Those  muscles  on  both  sides  of  the 
body  which  usually  act  together  have  especially  well  marked  bilateral  representation;  so  that 
these  muscles  are  rarely  completely  and  permanently  paralysed  in  unilateral  cerebral  lesions. 
A  cortical  paralysis  may  affect  motion  only  and  may  be  very  circumscribed;  two  or  three  fingers, 
or  the  thumb  only.  The  actions  which  are  especially  lost  in  the  cortical  lesions  are  the  purpose- 
ful actions  which  have  been  slowly  acquired  as  the  result  of  experience  and  training:  actions 
which  are  peculiarly  voluntary  and  skilful. 

A  destructive  lesion  of  either  of  these  types  of  motor  neurons  will  cause  a  motor  paralysis. 
If  the  peripheral  motor  neurons  are  destroyed  there  will  be  a  paralysis  both  of  voluntary  and 
of  reflex  acts:  a  flaccid  paralysis  (252),  while  if  the  central  motor  neurons  are  destroyed  there 
will  result  a  paralysis  of  voluntary  acts  only;  the  reflex  acts  persisting  and  being  even  increased: 
a  spastic  paralysis  (253).  (For  explanation  of  the  increase  of  reflex  activity  just  mentioned 
see  page  22.) 

The  Will  and  Will  Power 

The  term  "voluntary"  motion  implies  "volition"  or  "will":  some  attribute  of  the  individual 
or  personality  which  controls  or  regulates  the  cerebral  activities.  The  will  and  the  freedom  of 
the  will  stand,  however,  in  direct  contradiction  both  to  the  law  of  preservation  of  force  or  energy 

24 


and  to  the  law  of  causality.  Moreover,  we  have  just  learned  on  page  23  that  voluntary  motion 
results  from  the  play  of  motives  and  that  the  strongest  sensory  cortical  activity  prevails  and 
causes  the  resulting  motion  which  seems  to  be  due  to  our  will  power  only  because  the  percep- 
tion or  memory  in  consciousness  resulting  from  this  "strongest  sensory  cortical  activity"  is,  in 
virtue  of  its  strength,  in  accordance  with  our  so-called  will  or  desire.  It  seems,  therefore,  better 
to  call  these  actions  which  result  from  the  strongest  sensory  cortical  activity  "association  re- 
flexes" rather  than  voluntary  acts.  As  the  result  of  experience  in  life  we  acquire  desires  (see 
page  11)  and  each  desire  can  only  be  satisfied  by  action.  The  presence  in  consciousness  of  a 
desire  to  obtain  a  certain  end  or  result;  which  desire  is  itself  the  result  of  cortical  activity  will 
by  this  intense  cortical  activity  excite,  influence  and  usually  control  those  cortical  activities, 
which  produce  action,  thought,  study,  etc.  It  is  the  cortical  activity  causing  the  desire  which 
does  this,  not  some  external  entity:  the  will. 

The  act  of  concentration  or  attention  seems  also  to  call  for  a  will  power,  but  we  have  learned 
on  page  14  that  concentration  depends  primarily  on  a  strong  cortical  activity,  which  the  so- 
called  will  power  and  our  desires  are  often  incapable  of  controlling.  What  has  been  called  the 
will  is  probably  the  dominant  cortical  activity  present  in  consciousness  at  any  given  moment. 
It  depends  upon  the  personality  which  rests  upon  many  experiences  and  upon  many  crystal- 
lized experiences  in  the  form  of  judgments,  habits,  prejudices,  etc.,  which  give  our  actions 
stability  and  consistency;  and  this  sum  of  consciousness,  or  even  one  strong  idea  in  conscious- 
ness, the  result  of  a  strong  cortical  activity,  may  modify  the  association  of  ideas  and  may  control 
both  them  and  the  resulting  action. 

Nevertheless,  both  in  voluntary  actions  and  in  efforts  of  attention,  the  individual,  or  the 
personality,  does  not  seem  to  himself  to  be  a  mere  passive  spectator,  but  feels  that,  although  he 
may  be  somewhat  bound  down  by  experience  and  habit  and  prejudice,  yet  he  does  exercise  a 
very  real  and  decisive  influence  upon  both  these  processes,  and  at  least  modifies  if  he  does  not 
actually  control  them.  Everyone  feels  conscious  of  this  power,  and  it  is  not  altogether  satis- 
factory to  dismiss  this  feeling  as  a  delusion  existing  in  the  mind  of  every  member  of  the  human 
race.  It  is  indeed  quite  possible  that  the  personality,  which  is  a  force  produced  by  chemical 
process  taking  place  in  the  sensory  cerebral  cortex:  the  result  of  cellular  activity,  may  in  the 
motor  cortex  be  transmuted  back  into  cellular  activity,  and  thus  may  promote  or  inhibit  motor 
action.  Just  as  an  electric  light,  produced  by  chemical  activity  within  a  battery,  may  be  trans- 
muted again  upon  a  photographic  plate  into  chemical  action;  or  as  the  light  of  the  sun  acting 
upon  the  chlorophyl  in  green  leaves  may  break  up  the  molecule  of  carbon  dioxide  into  its  con- 
stituent parts:  carbon  and  oyxgcn. 

Personality  is  a  force,  and  it  is  hard  to  conceive  of  an  immaterial  spirit  as  anything  else 
than  a  force  The  primary  and  essential  element  in  the  process  still  remains  the  activity  of  the 
neuron,  and  we  have  already  seen  that  the  force  generated  by  one  set  of  neurons  may  in  turn 
generate,  or  modify,  the  activity  of  another  set  of  neurons.    Thus,  the  personality,  which  is 

gradually  built  up  during  the  life  of  an  individual,  may  play  an  active,  not  a  passive,  role  in  the 
phenomena  constituting  his  conscious  life  and  activity.  This  statement  of  what  constitutes 
the  will  and  will-power  is  in  harmony  with  the  subjective  feelings  of  mankind;  and  yet  it  is  but 
a  restatement  in  other  words  of  what  has  been  said  in  the  preceding  paragraph  that  "  the  will 
is  the  dominant   cortical  activity  present   in  consciousness  at   any  given  moment,"  because  the 

personality  is  also  the  expression  of  the  sum  of  the  cortical  activities  present  at  any  given  moment. 

Spasms  am>  Convulsions  (Chabt  iy> 

Spasms  and  convulsions  consist  in  involuntary  muscular  contraction.    They  depend  mainly 

upon  irritation  of  the  central  ^ray  matter,  especially  the  cerebral  cortex,  and  partly  upon  peri- 
pheral  irritation. 

Passive  contract  lire  and  Thomsen's  disease  alone  are  purely  of  peripheral  (mUSOUlax)  origin. 

Many  of  the  tonic  spasms  are  reflex,  some  are  the  result  of  nerve  root  irritation  (meningitis, 

tumor   .   etc.)    and    many   an    associated    with   defeneration   of   the   pyramidal    tract-. 

25 


The  result  of  pathological  and  experimental  investigation  makes  it  evident  that  epileptic 
and  epileptiform  convulsions  originate  from  irritation  of  the  motor  cortex.  When  a  slight, 
but  lasting,  local  irritation  of  the  motor  cortex  occurs,  there  results  a  local  spasm,  clonic  and 
tonic,  which  extends  from  one  extremity  to  another  and  finally  becomes  a  general  convulsion, 
accompanied  in  some  cases  by  coma.  When  the  irritation  is  stronger  and  especially  when  it 
affects  both  hemispheres  there  results  first  a  tonic  followed  by  a  clonic  convulsion  and  coma. 
Irritation  of  other  parts  of  the  cortex  can  also  produce  epileptic  convulsions,  if  the  irritation 
be  strong  enough  and  the  motor  cortex  be  intact.  Tonic  spasms,  without  clonic  ones,  may  be 
obtained  by  irritation  of  many  parts  of  the  central  nervous  system.  The  epileptiform  convul- 
sion caused  by  cortical  irritation  may  be  accompanied  by  alterations  in  the  cardiac  action  in 
the  respiration  and  in  the  activity  of  other  internal  organs,  as  in  cases  of  ordinary  epilepsy. 
Indeed,  these  changes  in  the  cardiac  action  and  in  the  circulation  through  the  brain  may  be 
more  essential  factors  than  is  the  cortical  irritation  in  the  actual  production  of  an  epileptic  attack. 

The  contractures  which  accompany  cerebral  paralyses  are  due  to  contraction  of  the  stronger 
muscles,  partly  in  efforts  for  voluntary  movements  from  the  brain,  but  mainly  reflexly  from 
the  spinal  cord. 

The  pathogenesis  of  many  spasms  and  the  localization  of  their  origin,  especially  of  the 
irregular  spasm,  are  given  in  the  chart. 

The  various  forms  of  spasms  are  at  times  quite  difficult  to  recognize.  It  requires  much 
experience  to  be  able  always  to  differentiate  clonus,  tics,  athetoid  and  choreic  spasms  from  one 
another  and  from  the  perversions  of  motion:  tremor,  ataxia  and  apraxia.  This  is  unfortunate 
because  the  diagnosis  by  these  diagnostic  charts  requires  that  the  symptoms  be  correctly  ob- 
served and  named.  The  student  should  compare  carefully  what  he  sees  with  the  definitions 
in  the  book  and  should  observe  as  many  cases  as  possible. 

Apraxia,  Ataxia  and  Tremor  (Chart  IVc) 

When  an  impulse  from  a  cortical  motor  center  passes  down  to  a  group  of  nerve  cells  in  the 
anterior  horns  of  the  spinal  cord,  it  causes  a  definite  synergic  contraction  of  a  number  of  mus- 
cles to  produce  the  movement  over  which  this  group  of  nerve  cells  presides.  As  soon  as  this 
movement  commences,  a  number  of  sensory  impulses  pass  from  the  muscles  and  joints  involved 
to  the  co-ordinating  centers,  especially  to  the  cerebellum,  and  the  movement  is  consequently 
co-ordinated  and  orderly.  This  co-ordination  of  movements  is  not  inborn.  It  is  acquired  by 
experience  and  practice.  The  movements  of  a  new  born  baby  are  always  ataxic.  When  the 
function  of  the  cortical  center  is  impaired  there  results  a  paralysis  or  an  apraxia  (loss  of  skill) 
according  to  the  degree  of  the  impairment  and  when  the  co-ordinating  apparatus  is  functionally 
impaired  there  results  ataxia.  In  either  case  awkward,  ill-adapted  and  uncertain  movements 
result.  There  is  asynergy  the  muscles  taking  part  in  the  movement  do  not  act  together 
at  the  proper  time  and  with  the  proper  relative  force  to  produce  an  orderly  movement. 

The  motor  apparatus,  together  with  its  sensory  regulation,  may  be  called  the  executive 
apparatus  and  it  may  be  disordered  in  various  ways. 

1st.  If  the  motor  portion  of  this  apparatus  be  injured  there  results  a  paralysis  or  paresis. 
See  Chart  IVa. 

2nd.  If  the  sensory  or  regulating  apparatus  be  injured  there  results  ataxia.  See  Chart 
IVc. 

3rd.  If  what  has  been  learned  has  been  lost  or  impaired  there  results  apraxia  or  dyspraxia. 
See  Chart  IVc. 

Ataxia:  inco-ordination  of  movement,  always  depends  upon  some  disturbance  of  the  sen- 
sory or  regulating  apparatus.  It  occurs  in  several  distinct  varieties,  depending  upon  the  por- 
tion of  the  sensory  nervous  system  affected. 

1st.     Peripheral,  or  dynamic,  due  to  lesion  of  the  peripheral  sensory  neurons. 

2nd.  Cerebellar,  or  static,  due  to  lesion  of  the  cerebellum  or  its  tracts,  including  the  termi- 
nation of  the  auditory  nerve  in  the  semi-circular  canals. 

26 


3rd.     Cerebral  ataxia,  to  a  lesion  of  the  cerebral  hemispheres. 

1.  Peripheral,  or  dynamic,  ataxia  (280,  644)  is  caused  by  an  impairment  or  loss  of  the 
complicated  sensations  conveyed  by  sensory  fibers  from  the  muscles,  joints  and  other  tissues  which 
is  known  by  the  name  of  muscle-joint  sense  (42  and  352).  It  affects  all  movements  of  the  parts 
involved.  It  is  associated  with  hypotonia  (240),  which  allows  an  abnormal  excursion  in  passive 
movements  without  the  resistance  normally  offered  under  sudden  stretching,  and  which  may 
allow  of  abnormal  positions  of  the  extremities.  The  loss  of  the  muscle-joint  sense  can  to  some 
extent  be  replaced  by  the  sense  of  sight,  which  allows  the  patient  to  guide  his  movements  by 
his  eyes. 

Cerebellar,  or  static,  ataxia  (281,  642)  is  caused  by  impairment  of  the  function  of  the  great 
co-ordinating  organ:  the  cerebellum.  It  affects  mainly,  or  only,  walking  and  standing,  which  acts 
resemble  those  of  a  drunken  man,  or  become  absolutely  impossible.  The  sense  of  sight  gives 
very  little  aid  in  such  cases.  Movements  of  the  extremities  while  the  patient  is  recumbent 
are  fairly  normal.  With  cerebellar  ataxia  is  usually  associated  vertigo;  although  this  latter 
symptom  may  not  be  pronounced. 

Cerebral  ataxia  is  due  to  a  lesion  of  the  sensory  tracts  and  centers  within  the  brain.  If 
this  lesion  involves  the  sensory  tracts  in  the  medulla  or  pons  or  crura  cerebri,  the  cerebellar 
tracts  may  also  be  involved  and  the  ataxia  may  be  either  cerebellar  or  dynamic  or  both.  In 
cases  of  cerebral  hemianesthesia  where  the  lesion  is  either  in  the  optic  thalamus,  the  internal 
capsule  or  the  parietal  cortex,  the  ataxia  which  invariably  results  is  of  the  dynamic  variety  and 
is  associated  with  hypotonia.  Such  cases  of  ataxia  may  be  slight  in  degree  and  may  show  great 
and  relatively  rapid  improvement.  When  the  lesion  is  in  the  parietal  cortex,  the  centers  for 
cutaneous  and  muscular  sensibility,  ataxia  results,  because  of  the  loss  of  those  sensations  which 
are  essential  for  the  proper  guidance  of  voluntary  movements.  In  tumors  of  the  frontal  lobe, 
whether  cortical  or  sub-cortical,  ataxia  is  a  common  symptom  and  is  of  the  cerebellar  type; 
being  doubtless  due  to  involvement  of  the  fronto-cerebellar  tract.  In  cerebral  ataxia  it  is  evi- 
dent that  the  patient  is  trying  to  execute  the  movements  and  knows  what  he  wants  to  do,  but 
he  executes  them  awkwardly. 

Apraxia  (282)  may  result  from  the  loss  of  the  purposeful  idea  which  should  prompt  a  given 
action.  In  lesions  of  the  posterior  central  convolution  or  of  the  supra-marginal  gyrus  this  idea 
cannot  be  formed  (sensorial  apraxia  or  agnosia),  in  which  case  the  action  which  should  follow 
the  idea  cannot  originate;  or  when  this  idea  is  formed  the  memory  is  quickly  lost  (amnestic 
apraxia),  in  which  case  the  appropriate  action  is  begun,  but  never  completed.  In  lesions  of  the 
anterior  central  convolution,  or  of  the  area  immediately  anterior  to  it,  the  purposeful  idea  may 
be  present,  but  the  innervation  memories  necessary  for  the  production  of  the  appropriate  action 
are  lost;  so  that  the  action  cannot  be  performed  (motor  apraxia).  When  the  association  libers 
connecting  the  anterior  and  posterior  central  convolutions  are  the  seat  of  lesions,  the  appropriate 
action  will  not  occur,  or  a  somewhat  similar  action  may  be  substituted  for  it  (associative  apraxia). 

In  any  organized  society  much  results  from  imitation  and  from  instruction.  Certain 
complexes  of  innervation  feelings  become  by  practice  so  firmly  united,  that  what  was  at  first 
done  with  difficulty  and  imperfectly,  becomes  easily  and  perfectly  done.  These  innervation 
complexes  are  not  inborn  (although  their  anatomical  Bub-Structure  may  well  be),  but  are  learned, 

are  acquired  by  practice.  These  innervation  complexes  become  memories  (kinesthetic  mem- 
ories). Innervation  memories  may  be  conscious  in  early  life  when  first  learned,  but  may  be 
Unconscious  ladr.      Many  of  them  may  never  enter  consciousness.      As  long  as  these  memories 

persisl  the  corresponding  action  may  be  performed,  consciously  or  unconsciously,  as  the  final 

result   of  sensory  impulses  exciting  them.      Many    complicated    acts    are    not    performed    often 

enough  to  form  an  innervation  complex,  but  must   be  performed  consciously  and  with  constant 

guidance  from  many  parts  of  the  brain  simultaneously  (sight,  muscle  sen -e,  touch,  etc.). 

Trttnor  (250)  may  bfl  camed  by  rapid  rhythmical  interruptions  of  the  innervation  impulses 

-  to  the  muscles  or  by  B  failure  of  a  proper  proportion  or  equilibrium  m  the  innervation 

of  the  muscles  and  their  antagonists.      Tremor  usually  ceases  during  sleep  and  is  usually  in 

27 


by  mental  excitement;  although  a  very  powerful  emotion  may  arrest  the  tremor  temporarily. 
It  seems  to  be  always  of  central  origin.  Clonic  spasm  from  exaggerated  reflexes  must  not  be  con- 
founded with  a  coarse  tremor. 


Speech  (Charts  IVc  and  XIII) 

The  most  complicated  and  important  of  all  voluntary  acts  is  speech.  Speech  and  the  allied 
functions:  reading  and  writing,  are  peculiar  to  human  beings  and  are  the  result  of  much  instruc- 
tion in  the  line  of  imitation  and  study.  These  functions,  therefore,  depend  upon  a  healthy  brain. 
If  a  child  has  such  an  imperfectly  formed  brain  that  he  is  an  idiot  (743),  he  consequently  cannot 
speak.  The  perfection  and  content  of  speech,  reading  and  writing  depend  upon  education; 
being  more  imperfect  the  less  the  education  and  training  and  are,  therefore,  often  quite  abnormal, 
or  even  absent,  in  the  defective  and  feeble-minded  (750,  1088,  1092)  and  in  hysteria  (747-8) 
and  insanity,  especially  in  adolescent  insanity  (1096),  in  dementia  (1103),  in  coma  (745)  and  in 
insanity  with  diffuse  cortical  changes  in  the  speech  area  (1104). 

The  power  of  speech  is  of  enormous  importance  in  the  development  of  the  race.  It  is  the 
one  factor  which  has  enabled  the  human  race  to  so  far  outstrip  all  other  animals  that  it  seems 
to  form  an  entirely  different  order  of  beings  from  them.  The  spoken,  and  still  more  the  written, 
word  allows  man  to  make  his  own  all  the  experience,  knowledge  and  wisdom  of  his  ancestors 
and  contemporaries,  and  raises  him,  thus,  far  above  his  own  limited  individual  experiences. 

Like  all  knowledge,  the  art  of  speaking,  reading  and  writing  is  acquired  from  sensory  im- 
pressions. The  art  of  speech  is  derived  from  the  sense  of  hearing;  so  that  when  a  child  is  born 
deaf,  or  acquires  deafness  in  the  first  two  or  three  years  of  life,  he  is  also  dumb:  a  deaf  mute 
(744).  A  deaf  mute  can  be  taught  to  speak  only  very  imperfectly,  and  then  only  by  the  sense 
of  sight,  or  much  more  rarely  by  touch  (Helen  Keller).  The  art  of  reading  and  writing  is 
derived  partly  from  the  sense  of  hearing  and  mainly  from  the  sense  of  sight.  If  a  child  is  born 
blind,  or  acquires  blindness  in  the  first  few  years  of  life,  he  can  learn  to  read  only  books  printed 
in  a  peculiar  way,  and  then  only  by  the  sense  of  touch  and  hearing;  the  sense  of  touch  replac- 
ing the  sense  of  sight  in  these  cases. 

It  is  evident,  then,  that  the  perceptions  and  memories  of  spoken  words  are  of  fundamental 
importance  in  the  art  of  speaking.  These  perceptions  take  place  and  these  memories  are  stored, 
in  right  handed  persons,  in  the  posterior  half  of  the  left  superior  temporal  convolution  and  in 
the  posterior  portion  of  the  left  island  of  Reil  (Fig.  15) ;  so  that  lesions  of  this  area  cause  a  pro- 
found disorder  of  speech:  sensory  aphasia  (772).  From  this  portion  of  the  cortex  impulses  pass 
along  association  fibers  (the  fasciculus  uncinatus)  lying  in  the  external  capsule  to  the  base  of 
the  left  inferior  frontal  convolution  (Fig.  15)  and  to  the  anterior  portion  of  the  island  of  Reil. 
A  lesion  in  this  region  also  causes  a  profound  disorder  of  speech:  motor  aphasia  (771). 

The  distinction  between  motor  and  sensory  aphasia  is  not  always  easily  drawn.  In  some 
cases  when  a  patient  is  unable  to  speak  a  desired  word  it  may  be  very  difficult  to  decide  whether 
he  has  forgotten  the  innervation  memories  necessary  to  speak  the  word  (motor  aphasia — 221), 
or  has  forgotten  the  word  itself  (sensory  aphasia — 222).  In  the  latter  case  he  may  be  able  to 
repeat  the  word  when  he  hears  it  spoken.  Lesions  of  the  external  capsule,  in  which  run  the 
association  fibers  connecting  the  centers  of  sensory  and  motor  speech  (the  fasciculus  uncinatus), 
also  cause  a  profound  disorder  of  speech  (conduction  aphasia). 

Perceptions  of  written  or  printed  words  are  formed  and  their  memories  are  stored,  in  right 
handed  persons,  in  the  cortex  of  the  left  occipital  lobe,  and  from  this  area  impulses  pass  along 
the  association  fibers  lying  beneath  the  angular  gyrus  to  the  base  of  the  left  inferior  frontal 
convolution  and  the  base  of  the  left  middle  frontal  convolution,  where  are  stored  the  innerva- 
tion memories  of  speech  and  writing  respectively.  Therefore,  deep  lesions  in  the  region  of  the 
left  angular  gyrus  in  right  handed  persons  will  cause  a  complete  alexia  (773)  and  an  incomplete 
agraphia  (776).  The  area  of  the  cortex  in  the  left  hemisphere  described  above,  including  the 
bases  of  the  middle  and  the  inferior  frontal  convolution,  the  island  of  Reil,  the  posterior  half 

28 


of  the  superior  temporal  convolution  and  the  angular  gyrus  is  called  "the  zone  of  language" 
and  is  the  cortical  center,  or  psychic  center,  for  the  faculty  of  language. 

In  addition  to  its  cortical  center,  speech  depends  upon  the  integrity  of  the  muscles  and 
nerves  which  move  the  lips,  tongue,  soft  palate,  larynx  and  those  concerned  in  respiration.  In 
lesions  of  these  muscles  and  nerves  and  of  their  nuclei  in  the  medulla  and  pons  and  of  the  pyra- 
midal tract,  speech  may  be  abolished  (anarthria)  or  pronunciation  impaired  (dysarthria), 
whether  in  consequence  of  paralysis  or  of  inco-ordination,  or  of  spasm  (as  in  stuttering).  Read- 
ing and  writing  may  be  similarly  abolished  or  impaired  in  lesions  of  the  peripheral  nerves  or 
of  their  nuclei  in  the  optic  thalamus  or  in  the  anterior  horns  of  the  cervical  enlargement  of  the 
cord  or  of  the  fasciculus  of  Gratiolet  or  of  the  pyramidal  tract. 

Dysarthria  might  also  be  due  to  a  cortical  paralysis  of  the  pneumogastric  nerve,  but  the 
laryngeal  muscles  have  a  bilateral  cortical  representation;  so  that  if  one  cortical  area  be  injured 
the  corresponding  area  of  the  other  hemispheres  can  carry  on  the  function  of  speech  perfectly. 
There  is,  therefore,  no  laryngeal  paratysis,  or  consequent  dysarthria,  due  to  any  lesion  within 
the  cerebral  hemispheres,  unless  the  lesion  be  very  extensive  and  involves  both  hemispheres 
(pseudo-bulbar  paralysis). 

Automatic  Movements  (Charts  III  and  XVI) 

This  term  is  applied  to  two  quite  different  sorts  of  actions.  In  one  sense  automatic,  or 
autochthonus,  acts  are  reflex  acts  which  originate,  not  from  external,  but  from  internal,  or 
organic,  excitations  or  irritations.  One  of  the  best  examples  of  this  activity  is  the  respiratory 
act.     Such  acts  are  very  numerous  and  carry  on  the  nutritive  activities  of  the  body. 

The  name  is  also  applied  to  voluntary  acts  which  have  been  learned  with  more  or  less  diffi- 
culty, but  which  have  been  enacted  so  often  that  they  can  be  performed  without  consciousness. 
Such  acts  arc  walking,  writing,  piano-playing,  smoking  and  many  others  which  can  be  very 
perfectly  performed  unconsciously,  although  each  one  can  also  be  enacted  consciously  and 
usually  is  so  done. 

Trophic  INFLUENCES  (Chart  XVII) 

The  nervous  system  exercises  an  important  trophic  influence  over  many  of  the  tissues  of 
the  body,  in  addition  to  influences  over  their  blood  supply  through  the  vaso-motor  system. 
This  trophic  influence  can  be  divided  into  two  great  divisions,  motor  and  sensory.  When  the 
motor  nerve  cells  of  the  central  or  peripheral  motor  neurons  are  degenerated  or  destroyed  (a8 
in  lesions  of  the  nerve  fibers  or  of  the  motor  cells,  of  which  these  nerve  fibers  are  the  axons), 
the  nerve  fibers  springing  from  such  degenerated  cells  undergo  a  rapid  degeneration,  as  do  also 

the  muscles,  in  which  these  nerve  litters  terminate;  and  inearly  life  when  there  is  motor  paralysis, 
or  immobility  of  parts  of  the  body  from  any  cause,  these  parts  fail  to  grow  normally. 

When  the  sensory  nerves  are  degenerated,  as  in  syringomyelia,  myelitis,  tabes,  lesions  of 

the  spinal  ganglia  or  of  the  ganglia  at  the  base  of  the  brain,  etc.,  in  consequence  of  the  anes- 
the-i.i,  tin'  I. oily  is  no  longer  protected,  by  retlex  and  voluntary  acts,  from  the  many  traumatisms 
to  which  it  is  frequently  BUbjected  and  therefore  ulcerations,  arthropathies,  ulcerations  of  the 
Cornea   and  other  trophic   lesions  result. 

Some  of  the  ductless  glands,  especially  the  pituitary  and  the  thyroid,  when  hypertrophied 

or  atrophied  as  regards  their  glandular  structure,  also  produce  widespread   trophic  disorder-. 

Tut:  CeBEBRO-SpINAL    li.rin   (CHARTS   \lll    am.    XIX) 

The  central  nervous  organs  (brain  and  spinal  cord  i  are  bathed  in  a  fluid  called  the  cerebro- 
spinal  fluid.       This  fluid   is  secreted  or  transudes  from   the  choroid   plexus  within   the  ventricles 

of  the  brain  and  thus  may  contain  substances  which  are  in  the  Mood,  it  passes  out  of  the 
ventricles  at  the  inferior  angle  of  the  fourth  ventricle,  through  the  foramen  of  Magendii      It 

from  any  Cause  (tumor,  meningitis,  etc.)  the  foramen  of  Magnidir  is  occluded,  this  Quid,  con- 
stantly secreted,  oannol  excape  from  the  ventricles  and  dilates  these  cavities  more  or  l< 

29 


cording  as  the  sutures  of  the  skull  are  ossified  less  or  more  completely;  thus  producing  internal 
hydrocephalus.  The  cerebro-spinal  fluid  passing  out  of  the  foramen  of  Magendie  becomes 
the  sub-arachnoid  fluid,  which  lies  in  the  meshes  of  the  tissue  forming  the  deeper  layers  of  the 
arachnoid.  In  this  situation  it  can  receive  products  of  any  inflammation  of  the  meninges: 
albuminous  substances  (globulin)  and  cellular  structures  (leucocytes  in  acute,  and  lymphocytes 
in  chronic,  inflammations) ;  so  much  so  as  to  be  cloudy  or  even  purulent.  The  specific  germs 
of  the  various  forms  of  meningitis  can  often  also  be  detected,  as  well  as  blood  in  hemorrhage 
and  pus  in  abscess.  In  tertiary  and  quaternary  syphilitic  meningitis  the  Wasserman  reaction 
is  usually  positive. 

The  cerebro-spinal  fluid  is  obtained  by  lumbar  puncture  and  the  rapidity  of  its  escape  is 
evidence  of  the  tension  which  it  is  under,  which  tension  can  more  accurately  be  measured  by 
a  manometer.  When  the  cerebro-spinal  fluid  is  increased  in  amount,  as  in  meningitis,  or  when 
a  foreign  body,  as  a  tumor,  is  within  the  cranial  or  spinal  cavity  the  tension  of  the  fluid  is  usually 
increased.  The  examination  of  this  fluid  is,  therefore,  of  much  importance  in  disease  of  the 
cerebral  and  spinal  meninges  and  in  other  intra-cranial  and  intra-spinal  conditions. 

Electricity  ajjd  the  Nervous  System 

Nervous  conduction,  although  it  has  some  analogies  with  electrical  conduction,  is  due  to 
an  entirely  different  form  of  energy.  But  when  nervous  action  takes  place,  whether  in  a  peri- 
pheral nerve  or  in  a  central  ganglion,  there  always  occurs  an  electrical  current  through  the 
nerve  or  ganglion  in  the  opposite  direction.  So  constant  and  delicate  is  this  reaction,  that 
it  has  been  used  to  prove  the  presence  of  nervous  activity.  Moreover  the  electric  current,  both 
Galvanic  and  Faradic,  can  be  conducted  along  nerve  fibers,  and  changes  in  the  tension  of  elec- 
tricity so  conducted  in  the  nerve  fibers  cause  contraction  of  the  muscles  in  which  they  termi- 
nate; as  is  shown  in  Chart  VII.  The  muscle  fibers  also  respond  directly  to  changes  in  intensity 
of  a  galvanic  current,  but  not  to  those  of  a  Faradic  current. 

All  forms  of  electrical  energy  are  excitants  for  all  the  sensory  organs,  acting  not  so  much 
upon  the  end-organs  as  upon  the  nerves  themselves. 

Other  forms  of  electricity,  especially  static  electricity  and  high  frequency  currents,  are 
used  as  therapeutic  measures  but  have  no  diagnostic  value. 


30 


CHART  I 

Case-Taking 


METHODS  OF  EXAMINATION  OF  PATIENTS  SUFFERING  FROM  NERVOUS  DISEASES 

Errors  in  diagnosis  result  more  frequently  from  imperfect  observation  than  from  faulty 
reasoning. 

Data  derived  from 

f  QUESTIONING see  chart  I  a. 

INSPECTION see  chart  I  b. 

PALPATION 

PERCUSSION 

ELECTRICITY 

LUMBAR  AND  BRAIN  PUNCTURE. 

OPHTHALMOSCOPY 

LARYNGOSCOPY 

ITHERMOMETRY 


Methods  of  Examining  and  Testing 
Patients - 


see  chart  I  c. 


see  chart  I  d. 


31 


CHART  I  a 

Questioning 

Comprising  Numbers  1  to  18 

(Note) — The  examination  of  every  patient,  who  is  conscious  and  intelligent,  begins  with 
a  history  of  his  health  and  of  thai  of  his  ancestors.  This  is  an  importanl  source  of  information, 
although  usually  less  so  than  arc  the  results  of  the  physical  examination.  The  taking  of  a 
reliable  clinical  history  is  something  of  an  art,  but  at  best  we  arc  absolutely  dependent  upon 
the  truthfulness  of  the  patient,  as  we  rarely  have  means  to  check  his  statement-  by  informa- 
tion from  other  sources.  It  is  important  to  put  the  patient  at  his  ease  and  to  gain  his  confidence. 
The  patient  is  vitally  interested  in  bis  own  ease  and  it  is  best  to  let  him  tell  his  own  story  of 
his  illness  in  his  own  way,  without  interruption;  then  to  question  him  further  about  his  01- 
oess,  more  especially  and  fully  in  regard  to  the  organ  probably  affected,  bu1  also  concerning 

the  function  of  the  other  organs  of  the  body.  This  done,  he  should  be  questioned  as  to  his 
previous  illnesses,  occupations,  etc.,  and  finally  as  to  any  special  prevailing  illness  in  his  ancestors 
or  relatives.  It  is  importanl  to  ask  as  few  leading  questions  as  possible.  Questions  in  regard 
to  personal  habits  and  \renereal  diseases  should  only  be  asked  when  absolutely  alone  with  the 

patient,  and  then  in  a  manner  which  assumes  that  all  men  are  guiltv  of  indiscretions.      During 

our  taking  of  th^  clinical  history  we  should  have  the  patient  under  close  observation  and  can 

thus  form  a  good  judgment  as  to  his  manner  and  general  mental  and  physical  characteristics. 


33 


METHODS  OF  EXAMINATION  OF  PATIENTS  SUFFERING  FROM  NERVOUS  DISEASES 


QUESTIONING 
Methods  of  Testing 

1  Allow  the  patient  to  tell  the  story  of  the  illness  without  interruption.     Then 

History  of  pres-     ascertain  the  exact  date  and  manner  of  onset  (sudden  or  slow,  prodroraata, 
ent  illness.  etc.)  and  the  exact  sequence  of  symptoms.     Inquire  into  all  details  which  may 

(Chart  II)  concern    the    case     (headache,   pain,   paresthesias,   vertigo,   insomnia,   mental 

condition,  emotions,  memory,  special  senses,  paralyses,  spasms,  fits,  disturb- 
ances of  organic  reflexes,  loss  of  weight  and  strength,  etc.),  whether  of  recent 
or  of  old  date.  Seek  for  any  possible  cause  (injury,  poisons,  drugs,  infections, 
worry,  mental  or  physical  overstrain,  shock,  etc.).  Be  careful  not  to  suggest 
answers  to  nervous  people.     Inquire  into  previous  treatment  and  its  effect 


Family  and 
personal 
history. 

(Chart  II) 


Consciousness. 
(Charts  III  & 
XVI) 


4 

Sanity. 
(Charts  III  & 
XVI) 


Intelligence. 
(Charts  III, 
XIII  &  XVI) 


Ascertain  the  occurrence,  in  the  present,  or  a  past,  generation  of  the  family,  of 
any  nervous  diseases,  especially  the  neuroses  (neuralgia,  epilepsy,  hysteria, 
insanity,  suicide,  drunkenness,  etc.),  or  of  syphilis,  or  tuberculosis.  Inquire  as 
to  consanguineous  marriages.  Note  patient's  age,  full  address,  race,  his  mental 
and  physical  development  in  school  life,  occupation,  habits  (alcohol,  drugs, 
venery,  masturbation,  etc.),  dwelling  and  previous  illnesses,  such  as  rickets, 
infectious  diseases,  chorea,  fits,  tuberculosis,  syphilis  (use  discretion  in  this 
inquiry:  ask  about  sore  throat,  skin  rashes,  miscarriages,  etc.),  and  injuries 
at  birth  or  later.  Ascertain  the  condition  of  other  organs  (cancer  and 
tuberculosis). 

Patient  may  lie  in  a  stupor  and  make  little  or  no  response  to  questions,  noises, 
shaking,  pin  pricks,  or  strong  sensory  irritations  of  any  kind.  He  may  appre- 
ciate neither  his  surroundings,  nor  his  acts,  nor  the  time  and  place,  nor  his 
own  individuality.  He  can  remember,  after  recovery,  nothing  of  what  hap- 
pened while  he  was  unconscious.  There  are  all  possible  grades  in  impairment  of 
consciousness  from  complete  coma  to  a  slight  lack  of  attention  and  an  inability 
to  collect  his  thoughts.     This  can  be  learned  by  conversation  with  him. 

Patient's  conversation  and  manner  may  show  that  his  brain  acts  in  an  abnormal 
way  and  that  he  entertains  abnormal  perceptions  and  ideas  (hallucinations, 
delusions,  compulsory  acts  and  ideas,  etc.).  Ascertain  if  a  change  has  taken 
place  in  the  patient's  normal  mental  state,  and  when.  Note  whether  patient 
is  elated,  active,  loquacious;  or  dull,  inattentive,  sluggish,  distracted,  evasive, 
suspicious,  and  why.  Some  cases  may  require  prolonged  observation.  At 
times  irritating  questions  may  be  desirable,  in  order  to  excite  the  patient. 

In  testing  a  patient's  intelligence,  we  test  his  general  knowledge  by  asking  him 
to  name  the  different  days  and  the  different  months  and  by  arithmetical,  geo- 
graphical, political  and  historical  questions.  His  power  of  observation  by  show- 
ing him  a  number  of  things  and  asking  him  later  to  describe  them.  His  power 
of  attention  by  asking  him  to  add  a  long  column  of  figures  or  underscore  a  letter 
wherever  it  occurs  in  a  page  of  print.  His  power  of  comprehension  by  asking 
him  to  explain  something  he  has  read  or  heard.  His  association  of  ideas  by 
giving  him  a  word  and  asking  what  other  ideas  it  suggests  to  him.  His  mental 
reaction  time  by  the  time  he  takes  to  solve  problems,  or  to  name  an  object,  the 
picture  of  which  is  shown  to  him.     His  moral  sense  by  questions  in  ethics. 


Memory  and 
understand- 
ing. 

(Charts  III, 
XIII  &  XVI) 


Emotions. 
(Charts  III  & 
XVI) 


An  apparent  defect  in  intelligence  may  be  due  to  lack  of  attention,  or  may  be 
shown  by  further  questioning,  by  having  him  repeat  long  phrases,  execute 
verbal  and  written  commands  and  name  objects  shown  to  him,  to  be  due  wholly 
or  in  part  to  a  loss  of  memory;  either  general  (amnesia),  or  local  (aphasia), 
especially  to  a  failure  to  understand  what  is  said  to  him  (sensory  aphasia); 
while  reason  and  judgment  are  normal.  Test  memory  for  remote,  as  well  as 
for  recent,  occurrences.  Test  his  memory  of  statements  made  a  few  minutes 
previously,  or  of  events  of  the  day  before,  or  of  years  before. 

Patients  may  show  by  their  conversation,  if  suitably  guided,  or  by  their  manner, 
or  by  both,  whether  the}'  are  emotional  or  not.  The  emotional  state  of  the 
patient  and  the  mental  characteristics  discussed  just  above,  can  often  best  be 
learned  from  the  statements  of  friends  and  relatives.  Curious  fears,  the  so- 
called  "phobias,"  (235)  are  often  present. 

34 


Speech. 
(Charts  III, 
XIII  &  XVI) 


9 

Reading. 
(Charts  III, 

XIII  &  XVI) 
10 

Writing. 
(Charts  III, 

xni&xvi) 

11 

Stereognosis. 
(Charts  III, 
VI  &  XXII) 


12 

Sight. 

(Charts  VI  & 
XIV) 


13 

Color  sense. 

(Chart  VI) 

14 

Field  of  vision 
for  white 
and  colors. 

(Hemianopia) 

(Charts  VI 
A:  XIV) 


15 

Hearing  and 

tinnitus 

annum. 

a  VI  & 

X  1 V  | 


Hi 
Smell. 

VI  & 
XIV) 
17 
Taste. 

\   I    A 

MY, 
is 

Bleep. 


QUESTIOXIXG  (Continued) 

Patient's  speech  may  be  entirely  absent  (anarthria)  or  altered  and  very  defec- 
tive, i.e.,  rational  or  irrational;  there  may  be  limited  vocabulary  or  use  of 
wrong  word  (aphasia),  poor  articulation  (dysarthria),  tremor  in  voice,  monot- 
onous, scanning  speech,  omissions  of  syllables  and  words.  Speech  is  tested 
by  interrogation  and  spontaneous  (voluntary)  speech.  Test  also  patient's 
understanding  of  letters,  wrords  and  phrases  spoken  to  him,  his  executing 
spoken  and  written  commands,  his  picking  out  objects  named;  and  have 
patient  name  objects,  give  sequences,  i.e.,  numbers,  days  of  week,  months, 
etc.,  and  repeat  catch  phrases,  as  "Round  the  rough  and  rugged  rock  the 
ragged  rascal  ran,"  etc. 

Ask  the  patient  to  read  aloud,  even  short  sentences,  words,  or  letters  only. 
Note  any  defect  either  in  utterance  or  understanding. 

Ask  the  patient  to  write,  spontaneously,  from  dictation  and  from  copy.  Have 
him  write  the  names  of  objects  shown  him.  Note  any  defect  in  the  character 
of  the  writing  or  in  the  ideas  expressed. 

Ask  the  patient  to  name  objects  placed  in  his  hand,  his  eyes  being  shut,  after 
excluding  anesthesia.  Even  without  feeling  them  all  over  and  without  moving 
them  about  in  his  fingers,  a  normal  person  should  be  able  to  recognize  many 
objects  (metals,  cloth,  etc.)  merely  laid  against  the  .-kin  of  his  hand,  face,  foot, 
lips.  etc.  Stereognosis  may,  therefore,  in  exceptional  conditions,  be  tested, 
although  less  perfectly,  in  other  parts  than  the  hands. 

Ask  the  patient  to  read  small  print  or  Jaeger's  test  type  at  reading  distance  (10 
to  16  inches,  according  to  age,  refractive  conditions,  etc.)  and  Snellen's  test 
letters  at  twenty  feet.  If  patient  cannot  read  the  appropriate  line  at  I 
feet  the  loss  of  vision  is  expressed  by  the  number  of  feet  from  the  chart  at 
which  he  can  read  this  line  divided  by  twenty.  Thus  at  ten  feet  the  vision 
would  be  expressed  by  £#.  In  P'l:lt  defed  of  vision  the  patient  may  be  able 
to  see  only  dimly  the  hand  moved  before  his  eye,  or  may  only  be  able  to  dis- 
tinguish between  light  and  darkness. 

Ask  the  patient  to  match  different  colored  worsteds. 

Place  the  patient  with  back  to  the  window  or  light  and  have  him  close  his  left 
eye  and  with  his  right  gaze  at  the  observer's  left  eye.  Then  let  the  observer 
move  his  hands  about  in  a  plane  mid-way  between  himself  and  the  patient; 
so  that  each  should  see  the  hand  at  the  same  instant  as  it  comes  into  the  field 
of  vision.  The  observer  can  Bee  it'  the  patient's  eye  wanders  from  his  own  and 
recall  it.  Test  left  eye  in  same  way.  If  any  defect  in  field  of  vision  is  suspected, 
use  a  perimeter.  With  a  perimeter  not  only  the  field  of  vision,  but  also,  by 
using  different  colored  papers,  the  color  field  can  be  mapped  out.  Normally 
the  color  field  is  largest  for  blue,  then  for  yellow,  orange,  red,  green,  etc,  in 
the  order  named.  If  this  order  is  changed  there  is  said  to  be  an  "inversion  of 
the  color  fields"  (849).  Normally  the  lines  limiting  the  different  color  fields 
are  everywhere  separate  from  each  other.  If  they  touch  or  cross  there  is  "in- 
terlacing of  the  color  fields"  or  "dyschromatopsia"  (849). 

The  patient's  hearing  may  bi'  tested  by  voice,  watch,  or  tuning  fork.  He  sure 
there  is  no  wax  in  the  ear.    Galton's  whistle  should  be  used  for  testing  high 

and   low   notes.      Each   ear  should    be   tested   separately.      Hone   conduction    is 

tested  by  holding  watch  or  tuning  fork  firmly  on  skull.     Normally  a  tuning 

fork,   which,  held  on   mastoid   Ceases   to  be   heard,   can  still   be  heard   when   held 

dose  t"  meatus  (Rhine's  test).     Normally  a  vibrating  tuning  fork,  held  on 
.•enter  of  forehead,  is  heard  equally  in  both  ears.     If  heard  best  in  the  deaf 

ear  (positive)  the  lesion  is  m  externa]  or  middle  ear.     If  heard  best  in  the  nor- 
mal tive)    the    lesion    is   m   inner  ear  or  in   auditory  nerve   (Weber's 

We  also  ask  about  ringing  in  ears  (tinnitus  aurium). 

Ask  patient  to  name  from  its  odor  any  fragrant  substance  (such  as  a-afoetida, 
cloves,  peppermint,  etc)  held  for  a  moment  beneath  each  no~tril  in  turn,  the 
other  being  dosed,      Ammonia  ami  acetic  acid  should  not   be  used   in  tl 

Ask  the  patient  to  point  to  the'  name  on  a  printed  card  of  the  taste  of  a  stron.dy 
bitter,   sweet,   salt    or  sour  solution    t -lied    from    a    medicine   dropper,    or   a 

camel's  hair  brush,  to  one  side  after  the  other  of  the  protruded  ' 

le  should   be  well  Washed   belweell  each   tot. 

The  amount   of  sleep  which  the  patient   L'ets  in  i  he  twenty-four  hours  is  always 

an   Important   question.     Insomnia   (agrypnia)   is   present   in   many  nervous 

ad  ij  apt  to  be  exaggerated  bj    patients;  so  that  their  statements 

should  be  controlled,  when  possible,  by  those  of  the  nurses  or  relatives.    Many 

sympl  i  ially  fears,  are  worse  at  night ;  "  Pavor  noctumus  of  children." 


CHART  lb 
Inspection  (mainly) 

Comprising  Numbers  20  to  42 


37 


METHODS  OF  EXAMINATION  OF  PATIENTS  SUFFERING  FROM  NERVOUS  DISEASES 

INSPECTION 


Methods  of  Testing 

20  The  expression  of  the  patient's  face  indicates,  in  most  cases,  the  degree  of  his 
Facial  expres-         intelligence  and  his  emotional  state  (sad  or  gay  or  anxious),  and  also  may 

sion  and  gen-  suggest  the  presence  of   certain  diseases  and  conditions;    such  as  myxedema 

eral  appear-  and  cretinism  (1163-4),  acromegaly  (1183),  scleroderma  (1165),  exophthalmic 

ance  and  goitre  (1193),  paralysis  agitans  (677),  myasthenia  (553),  nasal  obstruction, 

behavior.  atheroma  of  temporal  arteries,  notched  teeth,  hazy  cornea,  and  the  saddle- 

(Charts  XVI  back  nose  of  syphilis,  etc.     His  general  appearance  and  behavior  often  indi- 

&  XVII)  cate  his  power  of  self  restraint  (inhibitory  power,  breeding),  or  the  existence 
of  hallucinations  (213)  of  sight,  hearing,  touch,  or  of  compulsory  acts  (218). 

21  The  walk  of  the  patient  may  suggest  the  presenoe  of  hemiplegia  (254),  para- 
Walk,  plegia   (257),  local  paralysis  (259),  ataxia  (motor  or  cerebellar)   (248),  spasm 
(Chart  XIII)  (242),  atony  (252),  paralysis  agitans  (677)  and  other  tremors  (250),  pseudo- 
hypertrophic paralysis  (500),  hysterical  paralysis  (527),  foot  drop,  (bilateral  in 
multiple  neuritis  and  lead  palsy,  unilateral  in  acute  anterior  poliomyelitis), 
weakness,  exhaustion,  etc. 

22  The  skull  should  be  observed  as  to  type  (brachy-  or  dolicho-cephalic,  round  or 
Skull.  long  heads),  size  (microcephalic  —  small,  macrocephalic  —  large),  rickets  (box 
(Chart  XVI)           shaped),    general    or   local   hydrocephalus    (bulging — posterior    or   anterior), 

fontanelles  and  sutures,  asymmetry,  tumors,  etc. 

23  The  spinal  column  should  be  observed  as  to  curvature  (angular  or  lateral), scoliosis, 
Vertebral  col-         kyphosis,  spina  bifida  (occulta),  deformity  (dislocation),  Pott's  disease,  tumor 

umn.  tenderness  (by  palpation),  etc. 

(Chart  X) 

24  Note  the  existence  of  arcus  senilis,  the  condition  of  pupils  (unequal,  anisocoria 
Eye.  (341),  myosis  (340),  mydriasis  (339),  and  irregularity),  the  presence  of  keratitis 
(Charts  V,  VI         or  iritis,  prominence  of  eyeballs,  nystagmus,  squint,  ptosis,  paralysis,  etc. 

&XIV) 

25  Note  whether  each  pupil,  the  other  eye  being  covered,  dilates  and  contracts  as 
Pupillary  reflex      the  eye  is  alternately  shaded  by  the  hand  and  exposed  to  light,  or  an  electric 

to  light.  light  is  flashed  into  it;  vision  being  constantly  fixed  upon  some  distant  object. 

(Charts  V  &  When  a  pupil  contracts  to  light  (direct  reflex)  the  pupil  of  the  other  eye  also 

XIV)  contracts  (consensual  reflex). 


26 

Hemiopic  re- 
flex. 

(Charts  V  & 
XIV 

27 

Pupillary  reflex 
to  accommo- 
dation. 

(Charts  V  & 
XIV) 

28 

Double  vision, 

diplopia. 
(Charts  VI  & 

XIV) 

29 

Secondary 
deviation  of 
the  sound  eye, 

(Chart  XIV) 

30 

Nystagmus. 
(Charts  IV  & 
XII) 


Note  whether  the  pupil  contracts  as  light  is  flashed  on  each  half  of  the  retina 
alternately.  A  ray  of  light  collected  by  a  lens  should  be  used  in  this  test. 
This  reflex  is  difficult  to  obtain,  and  not  entirely  reliable. 

Note  whether  the  pupil  dilates  when  the  patient  looks  at  a  distant  object  and 
contracts  when  he  looks  at  one  so  near  his  face  as  to  require  convergence  of 
the  eyes.  This  test  can  be  made  on  a  blind  man  by  having  patient  first  con- 
verge his  eyes  and  then  make  the  axes  of  his  eyes  parallel,  by  imagining  that 
he  is  looking  at  a  near  and  then  at  a  distant  object. 

Note  which  eye  deviates,  however  slightly,  from  the  direct  axis  of  vision  and 
which  eye  lags  more  or  less  on  movement  of  eyeballs  in  following  the  moving 
finger.  Place  a  colored  glass  before  the  affected  eye,  move  a  bright  object 
(candle)  throughout  the  field  of  vision  and  have  the  patient  note  the  relative 
position  of  the  two  images.  The  colored  image  will  of  course  be  the  one  seen 
by  the  affected  eye. 

Hold  a  card  close  in  front  of  the  sound  eye.  Have  the  patient  look  at  an  object 
so  held  that  the  weakened  muscle  must  be  brought  into  action.  The  sound 
eye  covered  by  the  card  will  be  observed  to  move  too  far  and  when  the  card 
is  removed  the  sound  eye  will  quickly  move  back  into  proper  position. 

The  oscillation  of  the  eyeball  which  constitutes  nystagmus  is  often  plainly  to 
be  seen.  Extreme  deviation  of  the  eyeballs  in  one  direction  or  the  other  makes 
it  more  evident,  and  at  times  demonstrates  a  nystagmus  not  otherwise  appar- 
ent. If  present,  nystagmus  is  usually  recognized  while  making  the  two  tests 
28  and  29.  It  should  not  be  confounded  with  the  irregular  jerky  motion  of 
a  weakened  ocular  muscle  attempting  to  move  the  eyeball. 

38 


31 

Tremor. 
(Charts  IV  & 

XII) 
32 
Convulsion 

and  spasm. 
(Charts  IV,  XI 

&XII) 
33 
Paralysis 

(motor). 
(Charts  IV,  X 

&  XIII) 


34 

Paresis. 
(Charts  IV,  X 
&  XIII) 


35 

M     jthenia. 

(Chart  IV) 

36 

Diadocoki- 

nesia. 
(Chart  IV) 
37 
Ankylosis. 


INSPECTION  (Continued) 

Note  any  tremor  of  lips,  tongue,  or  other  parts  of  the  body.  Note  its  frequency, 
amplitude,  its  relation  to  voluntary  movements  and  whether  it  is  associated 
with  muscular  rigidity.  In  testing  for  tremor,  ask  patient  to  hold  arms  ex- 
tended before  him  or  over  his  head  with  fingers  spread  and  motionless. 

Note  any  convulsion  (269),  spasm  (245-6),  contracture  (263-4),  athetosis  (271), 
choreiform  movement  (272),  etc.,  which  may  be  present.  These  various 
forms  of  spasm  are  often  difficult  to  recognize  and  differentiate  from  each 
other. 

Note  any  obvious  paralysis,  such  as  ptosis.  Note  tin-  naso-labial  fold  and  the 
height  of  the  angle  of  the  mouth  on  each  side.  While  under  close  inspection, 
patient  should  be  requested  to  execute  every  possible  motion:  i.e.,  wrinkle 
forehead  (look  upward,  or  open  eyelids  held  closed  by  observer),  frown,  open 
and  shut  each  eyelid,  move  eyeballs  up  and  down  and  to  either  side  (note 
whether  upper  eyelid  follows  eyeball  well  downwards),  whistle,  laugh,  distend 
cheeks,  raise  upper  lip  and  each  angle  of  mouth,  protrude  tongue  straight  and 
move  it  in  all  directions,  raise  uvula  in  phonation,  close  jaws  and  move  chin 
forwards  and  jaw  laterally,  contract  strongly  all  muscles  of  face  at  once,  move 
head  backwards,  forwards  and  towards  each  shoulder  and  shake  it,  bend  body 
in  all  directions,  raise  arms  vertically,  raise  shoulder,  adduct  and  abduct  arm, 
flex  and  extend  elbow,  wrist  and  each  finger,  spread  fingers,  adduct,  abduct, 
flex  and  extend  thumb,  pronate  and  supinate  forearm  while  elbow  is  flexed, 
stand  on  each  leg,  raise  body  on  tiptoes,  adduct  and  abduct  thigh,  flex  and 
extend  thigh,  leg,  foot  and  toes. 

Make  strong  resistance  to  above  mentioned  movements  while  patient  is  executing 
them:  i.e.,  pull  on  eyelids,  on  one  angle  of  mouth,  resist  movements  of  jaw,  or 
of  bending  head  or  body,  or  of  flexing,  extending,  adducting  anil  abducting 
joints,  compare  the  strength  of  the  paretic  muscle  with  that  of  a  similar  healthy 
one,  when  possible,  with  its  fellow  of  the  opposite  of  the  body.  For  future 
comparison,  etc.,  the  strength  of  the  paretic  muscle  can  red  by  dyna- 

mometers, of  which  the  most  practical  is  the  one  for  the  hand  grasp.  Or  suffi- 
cient weights  may  be  placed  on  hand,  foot  or  head  to  overcome  the  attempted 
movement. 

Note  whether  patient  tires  easily  on  rep.:. ted  or  continuous  activity  of  any  set 
of  muscles. 

Note  whether  patient  can  alternately  extend  and  flex  joints  quickly  and  repeat- 
edly.    Test  especially  rapid  alternate  supination  and  pronation. 


Note  whether  any  joint  is  rigid,  so  that  it  cannot  lie  moved.    Ascertain  the  cause 
of  the  rigidity,  whether  bony  union,  contracted  muscle  or  contracted  Boar 

tissue  (muscle,  ligament,  skin,  etc). 
Note  whether  any  muscle  is  contraotured  with  consequent  impaired  motility  of 
the  joint  and  whether  this  contracture  can  lie  overcome  by  force,  witli  or  with- 
(Charts  IV  &  XI)    out  etherization   (active  contracture),  or  not    (passive  contracture). 

39  Note  whether  muscles  are  linn  or  flabby,  and  whether  or  not  resistance  is  offered 

Muscle  'one.  to  rapid  passive  motions  of  joints  while  the  patient  tries  to  make  no  voluntary 

IV  &  X)    resistance.    Normally  there  is  slight  resistance.    In  disease  the  resistance  may 
l.e  altogether  absent  (atonia),  or  weak  (hypotonia),  or  strong  (hypertonia). 

Xote   whether  any   muscle  shows  atrophy  or  hypertrophy,  or  fibrillary  contrac- 
tions, or  if  there  is  any  arrested  development  or  trophic  lesion-  of  other  I 
(especially   ulcers,   herpes,   glossy   skin,   abnormalities   of  nails,   etc.). 

Xote  whether  complicated   movements  are  executed   in  an  orderly  manner  while 

the  patient's  eyes  are  closed.    Ask  patient  to  walk,  touch  point  of  nose  with 

finger  tip,  pick  up  objects,  writ.',  touch  knee  with  heel  of  other  foot,  hold   foot 

iii  one  position,  trace  a  circle  in  the  air  with  foot,  walk  backwards,  walk 

along  a  line,  stand  on  one  fool   alone,  or  on  both  feet   close  together,  either  side 

de  or  one  in  front  of  the  other  (Romberg's  symptom),  stand  on 

or  on   heels,  stand  oil  one  foot   and   trace  a  circle  Oil  the  tloor  with  the  toe  of   the 
Other   foot.      All  should    be   made   both   with  e\,s   o|vii   and   shut. 

Note  whether  patient,  with  hi-  eyes  shut,  can  tell  whether  his  joints  are  flexed 
tended,  or  can  duplicate  with  one  extremity  the  position  in  which  his 

other  is   placed.      Note  whether  he  0811  estimate   weights  correctly  or  can 

eight  loaded  ball*  correetlj      Note  whether  he  can  locate  hi-  extremities 
being  shut,  an  extremity  after   being  n 

about   is  held   in  one  position  and   he  is  told   to  turn  his  head  and  eyeb 

that  when  he  opens  hi   eyes  he  -hall  l.e  looking  directly  at  hi-  thumb  01 

lor.       When    he   opens    hi-  e\es    it    Will    be    plain    to  see    whether   they   are  directed 
riL'ht  or  not. 

39 


38 

Contracture. 


40 
Trophic 

XVII) 

•tl 

Co-ordination 

(Chart-  IV  A 
\  I  I 


42 

Muscle  and 
joint 

Deep  '  ti-ihil- 

lt  V     (l.athves- 

thesia,    I 
the 

VI  A 
\[li 


CHART  I  c 

Palpation  and  Percussion 

Comprising  Numbers  45  to  68 


II 


METHODS  OF  EXAMINATION  OF  PATIENTS  SUFFERING  FROM  NERVOUS  DISEASES 
PALPATION  AND  PERCUSSION 


45 

Circulation  and 

respiration. 
(Chart  XVII) 

46 

Pulse. 

(Chart  XVII) 

47 
Difficulties  in 

sensory 

testing. 
(Chart  VI) 


48 

Tactile  sen- 
sibility. 

(Charts  VI  & 
XIV) 


49 

Pressure  sense. 

(Chart  VI) 

50 

Painful  sen- 
sibility. 

(Charts  VI  & 
XIV) 

51 

Retardation  of 
conduction. 

(Chart.VI) 

52 

Persistence  of 
sensation. 

(Chart  VI) 

53 

Localization. 

(Chart  VI) 

54 

Double  sensa- 
tion and 
polyesthesia. 

(Chart  VI) 


Methods  of  Testing 
Note  the  color  of  the  skin,  the  pulsation  of  arteries  in  neck,  the  condition  of  the 
jugular  veins  and  the  frequency  and  regularity  of  respiration,  especially  Cheyne- 
Stokes'  respiration  (435),  whether  respiration  be  costal  or  abdominal,  or  dia- 
phragm be  immobile,  unilaterally  or  bilaterally. 

Note  pulse  of  patient  as  to  frequency,  volume,  tension  (best  tested  by  tonometer 
or  sphygmomanometer)  and  irregularity  in  rhythm  and  force. 

The  result  of  all  sensory  tests  (and  the  same  is  true  in  regard  to  tests  for  many 
mental  symptoms)  depends  upon  the  patient's  truthfulness.  Deception  is 
always  possible  and  even  with  the  most  truthful  patients  the  tests  require 
much  time  and  the  results  are  often  contradictory,  especially  so  in  excitable 
and  in  uneducated  patients,  who  cannot  fix  their  attention  continuously. 
Nothing  should  be  present  to  distract  the  patient's  attention  and  his  skin  should 
be  warm.  In  some  nervous  diseases  the  patient  has  occasional,  spontaneous 
sensations  which  interfere  with  the  tests.  Most  patients  under  the  education  of 
repeated  tests  become  more  acutely  sensitive.  On  the  other  hand,  tests  too  long 
continued  tire  the  patient  and  give  rise  to  contradictory  results.  It  is  to  be 
remembered  that  the  sensibility  of  the  skin  both  for  tactile  and  painful  impres- 
sions varies  greatly  in  different  parts  of  the  body  and  in  different  individuals. 

With  the  finger  tip  (or  with  a  smaller  and  lighter  object,  such  as  the  head  of  a 
pin,  a  camel's  hair  brush,  a  pledget  of  cotton,  a  hair,  etc.),  touch  the  patient's 
skin  lightly,  having  told  him  to  say  "yes"  every  time  he  feels  the  slightest 
touch.  Or  the  patient  may  describe  figures  (space  sense)  traced  on  his  skin  with 
ink  (to  prevent  dispute  or  doubt).  A  pledget  of  cotton  is  better  for  accurate 
testing  than  is  the  finger  tip  or  a  pin,  because  with  the  cotton  the  pressure 
sense  (49)  is  eliminated.  Of  course,  during  all  sensory  tests  the  patient's 
eyes  must  be  closed  or  covered.  In  some  cases  of  hysterical  anesthesia,  if 
the  patient  is  told  to  say  "no"  when  she  does  not  feel  the  touch,  she  will  say 
"no"  only  at  the  instant  she  is  actually  touched  within  the  anesthetic  (?) 
area;  showing  that  sensation  is  not  abolished,  although  it  may  well  be  ab- 
normal. Tactile  sensibility,  or,  more  properly,  "space  sense,"  or  "localizing 
sense,"  (53),  may  also  be  tested  with  the  esthesiometer;  a  pair  of  blunt 
dividers,  by  which  it  is  noted  how  far  the  points  may  be  separated  and  yet 
be  felt  as  one.  This  distance  varies  greatly  in  different  parts  of  the  body  (at 
the  point  of  tongue  it  is  one  m.m.,  at  finger  tips  two  m.m.,  along  back  and  on 
upper  part  of  arm  and  thigh  it  is  sixty-five  m.m.  The  distance  is  smaller  trans- 
versely than  longitudinally  on  the  extremities.  Neither  this  compass  aesthesi- 
ometer,  nor  Herring's  aesthesiometer  gives  more  valuable  results  than  the  pin- 
head  tests.  When  mapping  out  an  anesthetic  area  commence  in  the  anesthetic 
area  and  work  towards  the  normal  skin.  Do  the  reverse  in  mapping  out  hyperes- 
thesia; i.e.,  from  normal  skin  to  hyperesthetic  area.  The  electro-cutaneous 
test  can  be  more  accurately  measured,  but  is  of  little  practical  value. 

Note  whether  patient  can  estimate  correctly  the  amount  of  pressure  exercised 
by  the  finger  pressed  against  the  skin,  or  by  weights  laid  upon  it. 

Note  whether  patient  feels  pain  when  pinched,  or  when  skin  is  pricked  by  finger- 
nail, pin-point,  or  other  sharp  substance.  Many  instruments  have  been 
devised  for  measuring  more  or  less  accurately  the  intensity  of  the  painful 
impression. 

Note  whether  the  painful  sensation  is  felt  immediately  upon,  or  some  seconds 
after,  the  painful  contact. 

Note  whether  the  painful  sensation  persists  a  longer  time,  after  the  painful  con- 
tact has  ceased,  than  is  normal. 

Note  whether  the  point  of  contact,  tactile  or  painful,  can  be  localized  correctly 
by  the  patient  either  by  description  or  by  pointing;  his  eyes,  of  course,  being 
shut. 

Note  whether  a  single  tactile  or  painful  contact  causes  two  (double  sensation)  or 
more,  sensations  (polyesthesia). 


42 


PALPATION  AND  PERCUSSION     (Continued) 

55  Touch  the  skin  at  numerous  points  alternately  with  small  test  tubes,  one  filled 
Temperature  with  hot,  the  other  with  cold,  water,  or  with  hot  and  cold  bodies  (spoons)  of  the 

sense.  same  size  and  form.    Certain  points  of  the  skin  are  especially  sensitive  to  heat; 

(Chart  VI)  others  to  cold.    It  is  well,  therefore,  to  test  for  heat  and  cold  separately. 

56  Note  whether  the  patient  feels  the  vibration  of  a  tuning  fork  (vibration  sense) 
Pallesthesia.  pressed  so  firmly  on  the  skin  that  the  vibration  can  be  transmitted  through 
(Chart  VI)  the  underlying  bone  (osseous  sense). 

57  Stroke  or  scratch,  as  softly  as  will  suffice,  with  finger  nail  or  head  or  point  of 
Cutaneous  pin,  the  skin  of  the  sole  of  the  foot  (plantar  and  Babinski),  or  a  buttock  (glu- 

reflexes.  teal),  or  the  inner  side  of  thigh  (cremasteric),  or  the  side  of  abdomen  (umbil- 

(Chart  V)  ical),  or  the  hypochondrium  (epigastric),  or  interscapular  region  (interscapular), 

or    stroke    firmly  along  the  postero-internal  border  of  the  tibia  (Oppenheim's 

58  reflex)  and  note  the  resulting  movement.  The  muscle  itself  must  be  felt  and 
Mucous  mem-         watched  in  cases  where  the  resulting  contraction  is  too  slight  to  move  the  part. 

brane  renexes.fpoucn  ^.j^  fingeri  straw,  brush,  or  probe,  the  cornea  or  conjunctiva  (conjunc- 
(Chart  V)  tival),  or  mucous  membrane  of  nose  (nasal),  or  palate  (uvular),  or  pharnyx 

59  (pharnygeal),  and  note  the  resulting  movement. 
Vaso-motor 

reflexes.  Note  the  pallor  or  redness  of  the  skin,  also  rapid  changes  and  flushings  with  or 

(Charts V& XVII)  without  irritation,  such  as  scratching  with  a  pin  or  fingernail  (dermographia). 

60  With  leg  relaxed,  semi-flexed  and  well  supported,  strike  or  press  the  sole  of  the 
Ankle-clonus.  foot  quickly,  firmly  and  continuously  upwards  and  note  whether  the  foot 
(Charts  V&X)       oscillates  or  not.     This  clonus  occurs  at  times  spontaneously  when  the  toe 

and  not  the  heel  rests  on  the  floor  ("spinal  epilepsy"). 

61  While  patient  is  sitting  on  a  chair  with  legs  crossed,  or  better  on  a  table  with 
Knee-jerk.  legs  hanging  free,  or  is  lying  in  bed  on  his  back  with  knees  flexed,  strike  the 
(Charts  V&X)  ligamentum  patellae  a  sharp  blow  with  the  finger,  edge  of  hand,  book  or  percus- 
sion hammer  and  note  whether  the  foot  flics  forward.  The  amplitude  of  the 
excursion  of  the  foot  is  not  alone  a  safe  guide  to  infer  increase  of  knee-jerk,  but 
rather  its  vigor,  its  quickness,  and  the  presence  of  two  or  three  additional 
oscillations  as  the  foot  falls  back  again.  Even  a  continuous  oscillation,  or 
clonus,  occurs  in  some  cases  (the  so-called  "spinal  epilepsy").  More  common 
than  this  clonus  is  a  simultaneous  contraction  of  the  adductors  of  the  other 
thigh  when  the  knee-jerk  is  exaggerated.  In  order  to  obtain  this  reflex  the  ob- 
server must  make  sure  that  the  muscles  of  the  legs  are  completely  relaxed.  The 
extensor  femoris  muscle  must  be  observed  and  felt  in  those  cases  where  the 
resulting  contraction  is  too  faint  to  move  the  leg.  Knee-clonus  may  be 
obtained  in  suitable  cases  by  grasping  the  patella  from  above  and  pullim:  it 

Q2  sharply  downwards. 

Achilles  reflex.    While  patient  is  kneeling  in  a  chair  with  his  feel   projecting  free,    the    tendo- 

(ChartS  V  &  X)  Achillis  should  be  Strongly  struck  with  B  percussion  hammer  and  the  movement 
g,  of  plantar  flexion  noled.     Where  the  patient  cannot   kneel  the  leg  may  be  sup- 

r>         ,  ,     .  ported   in   any   position   which   relaxes   it    and   the  teiido-Achillis  struck. 

reflex.  When   the  dorsum  of  the  foot  is  struck  sharply  over  the  4th  or  5th  metatarsal 

(Chart  V)  hones,    note    the    dorsal    (normal)    or   plantar    (pathological)    flexion   of   toes 

t;1  (Mendel-Bechterew's  reflex — 320). 

Elbow  and 

I    reflexes. The  arm  helm,'  relaxed,   well  supported  and  semi-llrxed   at   elbow  the  tendons  at 
(Chart  V)  elbow  or  wrist  are  sharply  struck. 

65  Tlie  patient's  ohm  is  firmly  grasped  with  finger  and  thumb  or  a  Hat  stick  is  placed 

The  jaw  nflex.       iii  thc>  patient's  Tin  nit  li  resting  on  his  lower  teeth,  the  mouth  being  half  open, 

(Chart   V)  and   then   the  stick  or  the   hand    holding  chin   is  .-truck  sharply  downward   and 

aa  the   Closure   Of   the   mouth   noted. 

Kernig's  reflex.  With  thigh  flexed  at  hip  and  leg  Hexed  at  knee,  the  patient  either  sitting  or  lying, 
(Chart*  V  &  X)  the  leg  should  be  quickly  extended  at  knee  join!  and  a  strong  resistance  to 
,.-  such  extension  noted,  it'  pit 

Mechanical  Strike  the  nerve  or  muscle  sharply  with  the  finger  or  permission  hammer  or  press 

irritability.  the  nerve  trunk  or  its  t. aider  points. 

88  The  tendon,  and  to  some  extent  the  cutaneous  reflexes,  can  be  made  stronger 

Reinforcement,      and  oan  be  often  made  to  appear  when  apparently  absent,  by  diverting  the 

patient's  attention  in  any  way,  usually  by  having  him  pull  strongly  on  his 
•  d  hands,  hi  eyes  being  turned  to  the  oeiling  or  to  a  picture  at  the  instant 

the  reflea  is  tested  (Jendre 

18 


CHART  I  d 

Electricity,  Lumbar  Puncture,  Brain  Puncture,  Ophthal- 
moscopy, Thermometry,  Caloric  Reaction 

Comprising  Numbers  70  to  80 


METHODS  OF  EXAMINATION  OF  PATIENTS  SUFFERING  FROM  NERVOUS  DISEASES 
ELECTRICITY  AND  LUMBAR  PUNCTURE 


70 

Farad  ism. 
(Chart  VII) 


71 

Galvanism. 
(Chart  VII) 


72 

Muscle  and 

nerve. 
(Chart  VII) 


Methods  of  Testing 

The  electrodes  should  be  kept  well  moistened  with  warm  .salt  water  during  the 
testing.  The  larger  electrode  is  placed  on  sternum  or  back  of  neck  or  sacrum; 
while  the  smaller  electrode,  provided  with  an  attachment  for  making  and 
breaking  (opening  and  closing)  the  current,  is  placed  over  the  motor  point 
of  nerve  or  muscle.  The  secondary  current  of  a  faradic  battery  should  be 
employed  and  the  current  should  be  gradually  increased  in  strength  by  methods 
which  vary  in  different  batteries,  until  the  faintest  distinct  contraction  of 
the  muscle  occurs  whenever  the  current  is  suddenly  closed,  the  negative  elec- 
trode being  over  the  motor  point.  The  test  should  be  repeated  several  times. 
As  the  skin  becomes  moister  a  less  strong  current  becomes  necessarj'.  It  is 
important  to  make  sure  of  the  exact  position  of  the  motor  point  in  each  case 
by  some  preliminary  tests  and  not  to  let  the  electrode  slip  away  from  this 
point  during  the  testing. 

With  the  electrodes  arranged  as  above,  first  the  negative,  later  the  positive, 
electrode  should  be  placed  over  the  motor  point  of  nerve  or  muscle  and  the 
strength  of  the  current  slowly  increased  by  means  of  the  rheostat  until  the 
faintest  distinct  contraction  of  the  muscle  occurs  whenever  the  current  is 
closed.  The  strength  of  the  current  causing  this  contraction,  with  each  elec- 
trode in  turn  over  the  motor  point,  should  quickly  be  read  from  the  galvano- 
meter, even  before  the  needle  has  quite  ceased  its  oscillations.  In  the  same 
way  read  from  the  galvanometer  the  strength  of  the  weakest  current  which 
will  cause  the  faintest  distinct  contraction,  when  each  electrode  in  turn  is  on 
the  motor  point  and  the  current  suddenly  opened. 

In  all  cases  both  the  muscle  and  the  nerve  supplying  it  should  be  tested  both 
by  faradism  and  galvanism. 


73  Note  the  character  of  the  muscular  contraction,  whether  quick  or  sluggish  (de- 

Character  of  the     generative),  or  showing  any  peculiarity,  and  whether  it  is  unusually  persistent 


contraction. 
(Chart  VII) 

74 
Lumbar 

puncture. 
(Charts  VIII  & 
XIX) 


(myotonic),  or  whether  it  rapidly  grows  feebler  under  repeated  tests  (myasthenic). 

The  patient's  body  should  be  bent  strongly  forwards.  Patient  should,  if  possible, 
sit,  but  may  be  lying  down.  The  skin  having  been  thoroughly  washed  with 
alcohol,  a  horizontal  line  should  be  drawn  from  the  posterior  spine  of  one  ilium 
to  the  other  and  a  sterilized  fine  needle  three  or  four  inches  long,  preferably  of 
platinum  and  with  rather  a  short  bevel,  should  be  inserted  between  the  laminae 
of  the  vertebrae  immediately  below  or  above  this  horizontal  line.  The  needle 
may  be  inserted  in  the  median  line  or  a  little  to  one  side  of  it  and  pushed  steadily 
forward  and  slightly  upward  until  it  enters  the  arachnoid  sac  when  usually  the 
cerebro-spinal  fluid  will  escape  in  drops.  If  the  needle  be  pushed  too  far  it 
can  be  felt  as  it  strikes  the  body  of  the  vertebra  and  it  should  then  be  with- 
drawn about  half  an  inch.  It  is  rarely  necessary  and  sometimes  dangerous  to 
attach  a  syringe  and  aspirate  the  fluid.  If  the  needle  becomes  occluded  clear 
it  out  with  the  stylet.  It  is  better  not  to  withdraw  more  than  half  an  ounce 
of  the  fluid.  Note  the  rapidity  of  escape,  whether  by  drops  or  in  a  fine  stream 
(tension), its  appearance  (cloudy, bloody, purulent).  The  fluid  may  be  examined 
chemically  (for  albumen,  sugar,  cholin,  etc.).  A  portion  of  the  fluid,  especially 
that  containing  the  fine  coagulum  which  frequently  forms,  is  centrifuged,  the 
clear  fluid  is  carefully  poured  off  and  the  bottom  of  the  tube  scraped  and 
aspirated  with  a  capillary  pipette,  the  content  of  which  is  spread  on  a  slide, 
fixed,  stained  and  examined  for  cells  (lymphocytes,  leucocytes,  bacteria,  etc.). 
The  cerebro-spinal  fluid  should  also  be  tested  for  an  increase  of  globulin,  indica- 
tive of  the  presence  of  a  syphilitic  infection,  of  ancient  or  recent  date,  or  of  a 
meningitis,  according  to  the  method  suggested  by  Noguchi  (419).  After  lumbar 
puncture  patients  should  remain  quiet  in  bed  during  twenty-four  hours.  Even 
so,  they  are  apt  to  suffer  from  headache,  especially  if  much  fluid  has  been  with- 
drawn, or  withdrawn  too  rapidly.  Sometimes  the  nerve  trunks  of  the  cauda 
equina  are  injured,  causing  pain  in  the  legs,  but  such  pains  are  rarely  severe 
and  are  of  short  duration.  In  some  cases,  in  consequence  of  the  withdrawal 
of  the  cerebro-spinal  fluid,  the  medulla  and  cerebellum  have  been  drawn  down 
into  the  foramen  magnum  and  death  has  resulted  promptly.  Such  an  acci- 
dent is  only  possible  in  cases  of  cerebral  tumor  situated  in  the  posterior  fossa  of 
the  skull,  and  therefore  lumbar  puncture  should  not  be  performed  in  such  cases. 

46 


BRAIN    PUNCTURE,    OPHTHALMOSCOPY,    LARYNGOSCOPY,   THERMOMETRY,   AND 

THE  CALORIC  REACTION 

75  This  operation  consists  in  trephining  (with  avoidance  of  the  sinuses  and  large 

Brain  puncture  arteries)  a  small  button  from  the  scalp  and  bone,  inserting  a  very  thin  needle 
canula  and  aspirating  a  small  quantity  of  the  brain  substance,  or  tissue  of  a 
tumor,  or  fluid  from  a  cyst.  It  has  been  many  times  performed  and  the  results 
have  been  somewhat  encouraging,  but  it  is  an  operation  which  should  be  per- 
formed only  by  an  experienced  surgeon  or  neurologist  and  its  detailed  descrip- 
tion is  hardly  in  place  here. 


76 

Ophthal- 
moscopy. 
(Chart  XIV) 

77 

Laryngoscopy. 
(Chart  XIII)" 

78 
Thermometry. 


7!  i 
Caloric 

reaction. 
(Chart  XII) 


80 

Cerebellar 
nystagmus. 

(Chart    XXI; 
1272) 


Examine  the  eyes  for  choked  disc  or  optic  neuritis,  and  for  optic  atrophy,  reti- 
nitis, miliary  tubercles,  etc. 

Examine  the  larynx  for  evidence  of  paralysis  of  one  or  more  or  of  all  its  muscles. 

It  is  often  necessary  to  ascertain  the  temperature  of  the  patient.  The  thermom- 
eter should  be  well  washed  in  cool  water  both  before  and  after  taking  the  tem- 
perature. In  taking  the  temperature  in  the  mouth,  the  bulb  of  the  thermometer 
should  be  placed  well  under  the  tongue  and  it  should  be  noticed  that  the  lips 
are  held  tightly  closed  during  the  two  minutes  that  the  thermometer  is  left 
in  the  mouth.  In  taking  the  temperature  in  the  axilla,  the  axilla  should  first 
be  wiped  dry  from  sweat  and  care  should  be  taken  that  the  thermometer  be 
surrounded  by  skin  and  not  at  all  by  clothes;  the  patient  should  be  rolled  over 
on  his  side  in  order  to  press  arm  firmly  against  chest  and  the  thermometer 
should  be  left  in  position  eight  minutes.  In  taking  the  tem|x>rature  in  the 
rectum,  a  little  vaseline  or  soap-suds  should  be  put  on  the  bulb  before  inserting 
it  into  the  rectum,  where  it  should  remain  two  minutes.  Instruments  have 
been  invented  for  taking  the  surface  temperature  of  the  skin  of  any  part  of 
the  body,  but  they  have  not  proved  to  be  of  much  practical  value. 

When  one  ear  of  a  normal  person,  with  head  held  upright,  is  syringed  out  with 
cool  water  there  results  a  horizontal  and  rotatory  nvst agmus  towards  the  other 
ear;  when  water  warmer  than  the  body  is  used,  the  nystagmus  turns  towards 
the  syringed  ear.  This  reaction  does  not  occur  in  cases  of  destruction  of  laby- 
rinth, <>r  of   paralysis  of  the  vestibular  nerve. 

In  lesions  of  the  ri^ht  cerebellar  hemisphere,  nystagmus  to  the  right  may  only 
lie  M-ni.  or  may  be  made  more  marked,  when  the  patient  lies  on  the  left  side, 
and  vice-versa. 


17 


CHART  II 

Analysis  of  the  Subjective  Symptoms  of  the  Case 

Comprising  Numbers  81  to  190 


I-.' 


ANALYSIS  OF  THE  SUBJECTIVE  SYMPTOMS  OF  THE  CASE  (SEMEIOLOGY) 

List  of  diseases  most  likely  to  occur  as  the  result  of  the  etiological  factors  obtained  from  the 
history  of  the  case. 


'101  Idiocy  and  Imbecility 
102  Spina  Bifida  and  Meningocele 

103  Hereditary  (Huntingdon's)  Chorea 

84  Inherited 

Organic 

104  Hereditary  (Friedreich's)  Ataxia 

81  Heredity, 

Diseases 

Diseases 

105  Myatonia  Congenita 

including  con- 

106 Myotonia  Congenita  (Thomsen's  Disease) 

sanguineous 

107  Muscular  Dystrophies 

marriages  in 

^108  Syphilis  of  the  Nervous  System 

neuropathic 

families 

'109  Insanity 

(Predisposing 

110  Epilepsy 

cause) 

111  Hysteria 

85  Inherited 

Neuroses 

112  Chorea 

Tendencies 

113  Neurasthenia 

114  Neuralgia  and  Migraine. 
^115  Drunkenness  (Alcoholism) 

'116  Cerebral  Palsy  of  Childhood 

117  Acute  Anterior  Poliomyelitis 

118  Meningitis  (tuberculous,  etc.) 

Tnfancy  and 

Childhood 

119  Hydrocephalus 

120  Tetany 

And  all  the  inherited  diseases  except  103 
and  106 

121  Caries  of  Spine  and  Compression  Myelitis 

,86  Age 

122  Meningitis  (tuberculous,  etc.) 

' 

123  Hereditary  Ataxia 

Childhood  and 

124  Glioma 

Youth               -! 

125  Chorea 

126  Epilepsy 

127  Muscular  Dystrophies 

128  Hysteria 
.129  Insanity 

^Adult 

J 

All  other  forms  of  Nervous  Diseases  and 
many  of  those  above  given 

130  Hysteria 

'More  common     i 

131  Exophthalmic  Goitre 

in  women         1 

.  132  Neuroses 

82  Personal 

87  Sex 

Factors 

133  Locomotor  Ataxia  (Tabes) 

(Predisposing 

More  common     „ 

134  Paresis 

causes) 

.     in  men 

135  Injuries 
.136  Organic  Diseases 

r Jewish  &  Latin 

137  Neuroses 

88  Race 

-Anglo-Saxon 

138  Organic  Diseases 
'139  Beri-Beri 

89  Dwelling 

'Tropical               < 

140  Leprous  Neuritis 

Place, 

141  Sleeping  Sickness 

Habitation 

..Dampness 

142  Neuritis 

90  Occupa- 

(-Overstrain 

143  Occupation  Neuroses 

-    tions 

^Poisons 

144  Neuritis 
50 

r145  Wounds  and  Injuries 

146  Hemorrhage  in  Brain,  Cord  or  Membranes 

147  Meningitis 

'Physical 

148  Myelitis 

149  Disseminated  Sclerosis 

150  Neuritis 

151  Tumors 

'91  Trauma-     - 

.152  Abscess 

tism 

fl53  Hysteria 

Psychical,  Acute  J  154  Insanity 

&  Chronic         1 155  Neurasthenia 

v156  Traumatic  Neuroses 

83  Etiological 
Factors 
(Inciting 
causes) 


92  Poisons 
Toxic 


93  Infec- 
tions 


94  Syphilis 


rl57  Arsenical  Neuritis 
Metallic  J  158  Lead  Palsy,  Colic,  etc. 

1 159  Mercurial  Tremor 

Alcoholic  j  J60  Multiple  Neuritis 

( 161  Neurasthenia 

Tobacco,  Tea       f 162  Tremor 
or  Coffee  1 163  Neurasthenia 

Narcotic  164  Drug  Poisoning;  Acute  or  Chronic 

165  Neuritis 

166  Meningitis 
166  Myelitis 

Germs  and  J  167  Acute  Anterior  Poliomyelitis 

Toxines  1 168  Landry's  Paralysis 

169  Neuralgia 

170  Tetanus 
.171  Hydrophobia 

(172  Gumma 

173  Meningitis  Gummosa 

174  Neuritis  Syphilitica 

175  Endarteritis  Syphilitica 

\  176  Locomotor  Ataxia 
<  177  General  Paresis 

J 178  Neurasthenia 
1 179  Hysteria 


95  Exhaus- 
tion 


96  Extension 
Of  Inflam- 
mation 


Post-Syphilitic 
Infections 

From  Illness, 
Overstrain, 
Worry 

From  Venery 
and 
Masturbation 


Caries  of  Skull 
or  Vertebrae 


97    Arterial  I  H 

us  Metastasis  from  I  >ther 

Organs 


ISO  Neurasthenia 


f  ISl    Cerebral  or  Spinal  Abse. 

■  L82  Sums  Thrombosis 
is:;  Meningitis 
1st  Myelitis 

I  lv">   Neuritis 

186   tpopli 

mors 

(188  Tuberculous  and  Suppurative  Meningitis 


99  I H 
of  Other 
Organs 


Bright  'a  I  tiseasa     189  '  tamis 


j  Diabi 

I     Mellitus 


I '.in  Diabetic  Coma 


.inn  Cold  is  a  doubtful  direct,  but  probably  an  auxiliary  stioli 
51 


CHART  III 

Disturbances  of  Mental  Activity 


ANALYSIS  OF  THE  OBJECTIVE  SYMPTOMS  OF  THE  CASE  (SEMEIOLOGY) 
Definition,  Significance  and  Relationship  of  the  Symptoms  of  Disease. 


200 

Disturbances 
of  Mental 
Activity. 


201 

CONSCIOUSNESS 

The  appreciation  of  one's  existence  and ' 
individuality  as  separate  from  the 
rest  of  the  universe  (Subject  con- 
sciousness). The  content  of  conscious- 
ness is  the  sum  of  the  present  percep- 
tions of  the  various  sensations  (Object 
consciousness),  together  with  the 
memories  of  past  perceptions  and 
judgments  (Experience)  (Chart  XVI) 

202 
INTELLIGENCE 

The  power  of  ascertaining  facts  and  rea- 
soning upon  them.  The  power  of  dis- 
covering the  relation  of  things  and  of 
acquiring  knowledge  (Chart  XVI). 

203 

MEMORY 

The  power  of  retaining  in  the  mind  and 
of  recalling  at  will  perceptions  and 
ideas  formerly  received.  The  more 
striking  the  perception  and  the  more 
frequently  it  is  repeated  or  recalled, 
the  better  becomes  its  memory  (Chart 
XIII). 

204 
EMOTIONS 

An   emotion   is  a  state  of  conseioiisnesH 

accompanied  by  a  feeling  of  pain, 
pleasure,  fear,  anger,  wonder,  worn, 
etc  In  health  ■  person's  emotion  is 
usually  in  harmony  with  hie  environ- 
ment, bu1  in  diapasoH  may  be  quite  in- 
dependent  of  1 1 »« -  environment  (Chart 
XVI). 


In   disease,   consciousness   and   intelli- 
gence may  be  either  diminished  or 
perverted   as   is  set  forth   in 
Chart  III  a. 

Neither  intelligence  nor  consciousness  is 
exaggerated  or  increased  in  disease, 
although  the  latter  may  be  apparently 
so  (Self-consciousness).  In  such 
cases,  however,  there  is  a  concentra- 
tion or  limitation  of  consciousness 
rather  than  an  increase  of  it;  an 
exaltation  of  the  subject,  with  a 
lowering  of  the  object,  consciousness. 


In  disease,  memory  may  be  diminished 
in  whole  or  in  part,  and  the  emotions 
may  be  either  diminished  or  exagger- 
ated as  is  set  forth  in 
Chart  III  b. 

.Memory  is  never  increased  in  disease, 
although  certain  memories  may  be 
accentuated  and  others  lost. 


53 


CHART  III  a 

Disorders  of  Consciousness  and  Intelligence 

Comprising  Numbers  201  and  202,  and  205  to  218 


66 


ANALYSIS  OF  THE  OBJECTIVE  SYMPTOMS  OF  THE  CASE  (SEMEIOLOGY) 


201 
C 

0 

N 
S 

c 
I 

0 

u 

s 

N 
E 
S 
S 


Diagnostic 

Symptoms 

f205 

Coma 


CONSCIOUSNESS 


Definition 


The  patient  lies  in  a  profound  stupor  from 
which  he  cannot  be  aroused  by  irritation  of 
any  sensory  organ  (eye,  ear,  skin,  mucous 
membrane,  etc.)-  No  voluntary  acts  are  per- 
formed and  the  reflexes  are  abolished  or 
diminished,  except  the  circulatory  and  res- 
piratory, which  are  often,  but  not  always, 
deranged.  Patient  is  unable  to  swallow. 
Lips  and  cheeks  puff  out  during  expiration. 

206  The  patient  is  apparently  in  a  coma  but  by 

Semi-coma  strong  sensory  irritation  can  be  aroused  to 
or  some  manifestation  of  consciousness.     No 

Stupor  voluntary  acts  are  performed,  but  the  re- 
flexes are  usually  present.  Patient  can 
swallow.  Patient  may  lie  apparently  awake, 
but  really  unconscious,  with  a  low  mutter- 
ing delirium  (Coma  vigil). 
207 

Dazed,  Be-  The  patient  lies  in  a  deep  sleep  or  moves 
wildered,  about  automatically.  Can  be  rather  easily 
Somno-  aroused,  but  does  not  fully  appreciate  his 
lence  or  surroundings.  Can  speak  more  or  less  in- 
Sopor  telligently. 


Significance 
These  three  conditions  are 
not  always  sharply  differ- 
entiated, but  may  merge 
into  each  other.  They 
are  due  to  loss  or  di- 
minution of  brain  func- 
tion in  consequence  of 
pressure  upon  the  brain 
or  of  circulatory  dis- 
turbances in  it,  or  of 
poisons,  etc.  Occur  in 
traumatism,  and  in  many 
organic  diseases  of  the 
brain  and  its  membranes 
and  especially  of  its  blood 
vessels;  also  when  toxic 
substances  (morphia, 
etc.)  or  toxins  (fever, 
etc.)  are  in  the  blood; 
also  in  Bright 's  disease 
and  diabetes  mellitus. 
Rarely  the  condition  is 
functional. 


f208 
Erroneous    A  mental  condition  in  which  a  person  imagines  himself 
personal-     to  be  different  from  what  he  really  is ;  sometimes  an 
ity  animal,  sometimes  a  famous  character  in  history, 

sometimes  God,  etc. 


P 
E 
R 

V 

E  -I 

R 

T 

E 

D 


209 

Double 
personal 


210 

Auto- 
matism 

Somnam- 
bulism 


At  intervals  the  patient  is  in  a  sort  of  somnambulistic 
state  and  presents  an  abnormal  consciousness  and 
personality.  His  memory  at  times  changes  with  his 
personality,  in  which  case  he  remembers  only  occur- 
ences in  former  similar  conditions  and  not  those  of 
his  normal  state,  and  vice  versa.  This  is  a  very  rare 
condition  and  offers  much  opportunity  for  decep- 
tion, and  in  some  cases  of  hysteria  may  well  be  sug- 
gested by  the  examining  physician 


Occurs  in  insanity 
(functional). 


Occurs  in  hysteria 
and  epilepsy 
(functional). 


A  person  performs  complicated  and 
apparently  intelligent  acts,  while 
suffering  from  loss,  or  great  im- 
pairment, of  consciousness,  and 
retains  little  or  no  memory  of  the 
acts  done. 


Brain  is  probably  anemic  or  ex- 
hausted, or  the  patient  is  under  the 
influence  of  a  great  emotion  (fright). 
Occurs  in  epilepsy,  insanity,  hyp- 
notism, and  rarely  in  hysteria  (func- 
tional) ;  not  uncommon  in  childhood 
during  sleep. 


56 


Diagnostic 
Symptoms 

211 

Amentia 


212 
Dementia 


f213 
Hallucina- 
tions 


INTELLIGENCE 

Definition 

Absence  or  defect  of  intelligence, 
which  is  congenital  or  is  acquired 
in  infancy  before  the  intelligence 
has  developed. 


Significance 

Due  to  a  malformed  or  diseased 
brain.  Occurs  in  idiots,  imbeciles 
and  feeble  minded  persons. 


Absence  or  defect  of  intelligence, 
which  is  acquired  in  later  life  in  a 
person  previously  intelligent. 


214 

Illusions 


215 

Delusions 


Due  to  atrophy  or  functional  failure 
or  diminution  of  blood  supply 
of  cerebral  cortex.  Occurs  in  in- 
sanity and  is  often  its  terminal 
stage. 
Vivid  perceptions  of  sensations  (visual,  auditory,  ol-~ 
factory,  tactile,  painful,  etc.)  not  directly  dependent 
upon  any  external  corresponding  reality;  a  sensation 
without  an  external  object.  The}'  are  usually  re- 
garded as  real  and  are  then  associated  with  defective 
judgment  and  mental  impairment,  and  therefore 
cannot  be  corrected. 


Erroneous  perceptions.  A  false  interpretation  of  an 
actual  sensation,  which  is  really  of  a  different  nature 
from  that  which  the  patient  believes  it  to  be.  Fre- 
quently occur  in  rational  persons,  especially  in  those 
with  defective  terminal  sensory  organs.  In  such 
cases  easily  corrected. 


216 

Hypochon 
driasis 


217 

Delirium 


Erroneous  judgments  (often,  but  not  always,  depen- 
dent upon  hallucinations)  which  can  be  corrected 
neither  by  reason,  nor  by  the  evidence  of  the  senses 
and  which  are  not  in  accord  with  universal  human 
experience,  and  are  the  consequence  of  mental  cn- 
feeblement.  Delusions  are  systematized  or  un- 
systematized according  as  they  are  supported  or 
explained  by  more  or  less  coherent  reasoning,  or 
not.  The  systematized  delusions  are  of  much  more 
serious  prognosis. 

Delusions  of  imaginary  symptoms  and  illness  formed 
on  an  insufficient  basis  of  abnormal  sensations,  which 
cannot  be  corrected  and  are  associated  with  much 
mental  depression. 

Irrational  talk  in  persons  with  diminished  COnSCioUS- 
11688.  Probably  due  in  most  eases  to  hallucina- 
tions, illusions  and  mental  confusion;  consequently 
its  irrationality  may  be  in  part  only  apparent. 
Often  occurs  in  fevers. 


•J  is  Certain  thoughts  or  questions  or  doubts,  which  arefor- 

Compulsory     ever  in  the  patient 's   mind  ami    cannot    be  removed. 

ideas  and     They  may  be  of  any  nature.    Patients  are  irresistibly 
actions        compelled  by  an  unknown  force  to  « l < »  certain  acts  or 

(275)  to  say  certain  words,  usually  quite  trivial.     Patients 

hize  the  abnormal  character  of  these  ideas  and 

act,  and  are  made  very    unhappy   by    them,  but    are 
quite  unable  to  prevent  them. 

Methods  for  the  detection  of  disorders   "f   consciousness  and  intelligence  arc  desoribed  in 

Chart    la. 

POT  further  discussion  of  these  symptoms  and  the  which  they  occur  see  Chart  XVI. 


Due  to  disease  of 
the  cerebral  cor- 
tex, whether 
functional,  cir- 
culatory, toxic 
ororganic.  Usu- 
ally symptoms 
of  insanity,  or  of 
extreme  degree 
of  neurasthenia, 
are  also  present. 
In  insanity 
these  perver- 
sions of  intelli- 
gence cannot  be 
corrected  b  y 
jon  a  n  d 
demonstration, 
and  in  neuras- 
thenia only 
rarely  and  im- 
perfectly. 


:.7 


CHART  III  b 

Disorders  of  Memory  and  Emotions 

Comprising  Numbers  203  and  204  and  220  to  237 


59 


ANALYSIS  OF  THE  OBJECTIVE  SYMPTOMS  OF  THE  CASE  (SEMEIOLOGY) 


Diagnostic 
Symptoms 


MEMORY 

Definition 


'220  Inability  to  recall    former    perceptions   and 

Amnesia  ideas.    Loss  of  memory  in  general.    May  be 

more  or  less  extensive.    May  affect  memories 
of  the  immediate,  or  of  the  remote,  past. 

221  Inability  to  express  by  words  some  idea  in  the 

Motor  patient's  mind,  although  there  is  no  paraly- 

aphasia        sis  of  the  vocal  organs  and  the  patient  can 

usually  express  the  idea  by  gesture.    A  loss 

of  memory  of  how  to  speak  (innervation 

memories),  especially  names.    A  limitation 

goo  °f  tne  vocabulary. 

Sensory  or  Inability  to  understand  (although  not  deaf) 
Auditory  spoken  words  formerly  intelligible.  Loss 
aphasia  of  memory  of  words  formerly  heard.  Hence 
(word  inability  to  recognize  them  when  spoken 

deafness)      (233). 


203 
M 
E 
M 
0 
R 
Y 

D 
I 

M 
I 

N 
I 
S 
H 
E 
D 


223 

Optic] 
aphasia 

224 

Mixed 
aphasia 

225 

Paraphasia 
(Jargon 
speech) 

226 

Paragraphia    a  word,  or  the  placing  of  the  right  word  in 
the  wrong  place,  in  writing. 

227 

Agraphia 


Inability  to  name  objects,  which  the  patient 
sees  clearly,  although  he  can  name  them 
after  feeling  them.  Loss  of  visual  memo- 
ries (232). 

A  mixture  of  the  three  forms  of  aphasia  just 
described. 

The  use  of  a  wrong  word,  or  the  omission  of  a 
word,  or  the  placing  of  the  right  word  in  the 
wrong  place,  in  speaking,  with  consequent 
incoherent  speech.  Jargon  speech  is  an 
extreme  degree  of  this. 

The  use  of  a  wrong  word,  or  the  omission  of 


Inability  to  express  in  writing  the  idea  in  the 
patient's  mind,  although  he  formerly  could 
do  so  and  his  right  arm  and  hand  are  not 
paralysed. 

228  Inability  to  read  words  patient  could  formerly 
Alexia  read,  although  he  sees  them  clearly  and 

(Word  there  is  no  paralysis  of  his  vocal  organs, 

blindness) 

229  Inability  to  recognize  objects  by  the  sense  of 
Astere-  touch,  although  there  is  no  anesthesia  pr- 
ognosis        sent  in  sufficient  degree  to  prevent  it. 


230  Inability  to  execute  a  desired  act.     Loss  of 
Apraxia  skill  in  executing  acts,  although  there  is  no 

motor  paralysis  present.  Loss  of  innerva- 
tion memories  necessary  to  perform  these 
acts. 

231  Inability  to  recognize  objects  through  some 
Agnosia  organ  of  sense  which  is  itself  normal.    This 

may  be  due  to  failure  of  full  perception  or 
to  loss  of  special  memories. 

232  Inability  to  recognize  well  known  objects  or 
Psychic  to  comprehend  familiar  things  by  sight,  al- 

blindness     though  the  patient  is  not  blind.     Loss  of 
visual  memories,  optic  aphasia  (223). 

233  Inability  to  recognize  and  comprehend  well 
Psychic  known    words   and   sounds,    although   the 

deafness       patient  is  not  deaf.  Loss  of  auditory  memo- 
ries.    Includes  sensory  aphasia  (222). 

60 


Significance 
Functional  or    organic  dis- 
ease of  the    cerebral  cor- 
tex, often    anemia,  some- 
times the  result  of  fright. 

Lesion  in  or  near  base  of 
left  inferior  frontal  con- 
volution and  anterior  por- 
tion of  left  island  of  Reil 
in  right 'handed  persons, 
and  of  the  right  side  in 
left-handed  persons. 

Lesion  in  or  near  posterior 
part  of  left  superior  tem- 
poral convolution  and 
posterior  portion  of  left 
island  of  Reil  in  right 
handed  persons. 

Lesion  of  left  occipital  lobe 
or  of  association  fibers 
from  this  lobe  in  right 
handed  persons. 

Any  one  or  a  combination 
of  the  above  lesions,  or  a 
lesion  of  the  island  of  Reil, 
or  of  external  capsule  in 
right  handed  persons,  in 
whom  the  above  lesions 
are  always  in  the  left 
cerebral  hemisphere,  or, 
in  slight  degree,  may  re- 
sult from  carelessness. 

Lesion  in  the  base  of  the 
middle  left  frontal  convo- 
lution, cortical  or  sub- 
cortical. 

Sub-cortical  lesion  beneath 
left  angular  convolution 
in   right  handed  persons. 

Lesion  in  or  near  cortex,  or 
sub-cortex,  of  contralat- 
eral posterior  central  con- 
volution. 

Cortical,  or  sub-cortical, 
lesion  of  motor  area  of 
contralateral  hemisphere. 


Cortical,  or  sub-cortical, 
lesion  of  sensory  area  of 
cortex  of  contralateral 
cerebral  hemisphere. 

Cortical,  or  sub-cortical, 
lesion  of  left  occipital 
lobe,  except  in  region  of 
calcarine  fissure. 

Cortical,  or  sub-cortical, 
lesion  in  left  superior 
temporal  convolution  'n 
right  handed  persons. 


Significance 


EMOTIONS 
Definition 

Without  adequate  cause  the  patient  is  de- 
pressed and  unhappy.  There  is  a  great  re- 
pression of  mental  and  physical  activity 
usually.  He  can  be  influenced  little,  if  at  all, 
by  reason;  difficult  to  get  his  attention. 

Without  adequate  cause  the  patient  is  in  con- 
stant fear  of  an  impending  calamity,  or  has 
an  unformulated  fear.  He  dreads  to  cross 
an  open  space  (agoraphobia),  or  to  enter  a 
small  room  or  confined  space  (claustropho- 
bia), or  fears  a  storm  (astrophobia),  or  syph- 
ilis (syphilophobia),  or  ill-timed  urination 
(urophobia),  or  everything  (pantophobia), 
etc.  Can  be  influenced  little,  if  at  all,  by 
reason.  Frequently  has  a  more  or  less  un- 
conscious sexual  basis. 

Without  adequate  cause  the  patient  is  exhil- 
arated. There  is  great  exuberance  of  mental 
and  physical  activity.  Careless  and  destruc- 
tive Can  In'  influenced  little,  if  at  all.  by 
reason.    Difficult  to  get  his  attention. 

Without  adequate  cause  patient  is  in  a  dull 
stuporous  condition.  No  expression  of  phys- 
ical or  mental  activity.  An  automaton,  sub- 
mitting passively  to  whatever  is  done  for 

him. 

Methods  for  the  detection  of  disorders  of  memory  and  emotion  are  described  in  Chart  I  a. 
For  further  discussion  of  these  svmptoms  and  of  the  diseases  in  which  they  occur  see  Charts 
XIII  ami  XVI. 


Diagnostic 

Symptoms 

'234 

Sadness 

(Melan- 

cholia) 

'  E 

235 

X 

Fear 

A 

(Phobias) 

G 

G 

E  -i 

R 

204 

A 

E 

T 

M 

E 

0 

D 

T  - 

I 

236 

0 

D 

Joy 

N 

I 

( Mania) 

S 

M 

I 

- 

X 

I 

237 

s 

Apathy 

H 

1. 

D 

Functional  or  circulatory 
disturbance  of  cerebral 
cortex,  especially  cere- 
bral exhaustion.  Occurs 
in  neurasthenia  and  espe- 
cially in  insanity. 

Fears  and  apprehension 
seem  to  be  the  basic 
symptoms  of  many  forms 
of  incipient  insanity 
(Mosher). 


61 


CHART  IV 

Disorders  of  Voluntary  Motion 


ANALYSIS  OF  THE 
Definition,  Significance 


240 

DISORDERS  OF  VOL- 
UNTARY MOTION 

The  power  of  executing 
movements  by  an  effort 
of  will  is  acquired  in  early 
life.  The  process  is  quite 
obscure,  but  seems  to  de- 
pend upon  the  existence 
of  innervation  memories 
of  past  acts,  primarily  re- 
flex. Voluntary  motion 
depends  upon  the  integ- 
rity of  the  central  motor 
neurons  (461)  and  of  the 
peripheral  motor  neurons 
(462).  In  disease  the 
power  of  voluntary  mo- 
tion may  be  diminished, 
exaggerated  or  perverted. 

MUSCULAR  TONICITY 

Closely  connected  with  the 
power  of  voluntary  and 
involuntary  action  is  the 
fact  that  the  muscles  of  a 
normal  person  are  in  a 
condition  of  constant, 
slight,  but  varying,  con- 
traction. This  is  called 
muscular  tonicity  or  tone. 
It  is  really  a  reflex  act 
caused  and  maintained  by 
many  slight  irritations, 
and  can  be  abolished  by 
cutting  the  posterior 
nerve  roots.  Muscular 
tonicity  is  increased 
(hypertonia)  in  destruc- 
tive lesions  of  the  central 
motor  neurons  and  in 
some  functional  disorders. 
it  i  diminished  (hypo- 
tonia,) or  abolished  (ato- 
nia,)  In  destructive  lesions 
of   the    peripheral    motor 

or  sensory  neurons,  in 
lesions  of  I  be  cerebellum, 
m  sleep  and  in  narcosis 


OBJECTIVE  SYMPTOMS  OF  THE  CASE   (SEMEIOLOGY) 
and  Relationship  of  the  Symptoms  of  Disease. 
-  211 

PARALYSIS 

A  condition  in  which  the 
muscles  cannot  be  con- 


241 

DIMINUTION 
also  called 
AKINESIS  and 
HYPOKINESIS 


242 
EXAGGERATION 

also  called 

HYPERKINESIS 


243 
PERVERSION 

also  called 

PAR  ^KINESIS 


contracted  by  the  strong- 
est effort  of  the  will. 
As  commonly  used  the 
term  includes: 

PARESIS 

A  condition  in  which  the 
muscles  can  be  contrac- 
ed  only  feebly  by  the 
strongest  effort  of  the 
will. 

r245 

TONIC  SPASM 

A  continuous,  involuntary, 
muscular  contraction  of 
longer  or  shorter  dura- 
tion (572). 

246 

CLONIC  SPASM 

More  or  less  rhythmical 
alternations  of  involun- 
tary, coarse,  violent  mus- 
cular contractions  and 
relaxations  (571).  Must 
not  be  confounded  with 
a  coarse  tremor. 

247 

IRREGULAR  SPASM 
Involuntary  acts  of  various 
kinds  (292,  573-4). 

r248 
ATAXIA 

Disorderly  movements  due 
to  loss  of  power  of  co- 
ordination (638).  Asyner- 
gi:i.  Associated  with 
hypotonia  (252) 

249 

LOSS  OF  SKILL. 
LPRAXIA 

Awkwardness. 

260 
TREMOR 

involuntary  rhythmioal  os- 
cillal  ion  of  some 
the  bodj  or  of  a  muscle. 

I  e      powerful, more  rapid 

ami    more     rhythmical 

than  a  clonic  spusin   Kilt 

similar  in  appearance, 
especially  irhen  coarse. 
[Yemor  ma]  be  slow  (8 

to  Q  per  second  lor  rapid 
•     12     per 

It  may  l"-  coarse  or  line 


The  conditions 
under  which 
paralysis  or 
paresis  occur 
are  set  forth 
in 
Chart  IV  a. 


The  conditions 
under  which 
the  various 
forms  of 
spasm  occur 
are  set  forth 
in 
Chart  IV  b. 


The  conditions 
under  which 
t  he  various 
fornix  of  per- 
version        o  f 

motion  occur 

are    set    forth 

in 

Chart   I\   ■■ 


CHART  IV  a 

Motor  Paralysis 

Comprising  Numbers  244  and  251  to  260 


ANALYSIS  OF  THE  OBJECTIVE  SYMPTOMS  OF  THE  CASE  (SEMEIOLOGY) 


244  PARALYSIS  \  INTENT™11 


C 

H 

A 

R 

A  -{ 

C 

T 

E 

L  R 


Diagnostic 
Symptoms 

251  A 

Spastic,  or 
hyper- 
tonic, 
paralysis. 
(473). 

(Figs.  24-6) 


MOTOR  PARALYSIS 

Definition 

paralysis  in  which  the  muscles  show  in- 
creased tone  and  offer  much  resistance  to 
passive  motion,  especially  rapid  motion. 
The  normal  excursion  of  the  joint  is  re- 
stricted. The  muscles  have  their  normal 
volume   and   under   the    microscope   their 

fibers  show  a  normal  appearance.  The  elec- 
trical reaction  of  muscle  and  nerve  is  nor- 
mal (396).  The  tendon  reflexes  are  in- 
creased. 


Significance 

Destructive  lesion  of  cen- 
tral motor  neurons  (461). 
It  occurs  in  diseases  of 
the  brain  or  spinal  cord, 
or  may  be  functional. 
Rarely  a  reflex  spasm 
(268),  especially  preputial 
irritation  in  children,  or 
pain,  may  simulate  this 
condition. 


252  A 

Flaccid,  or 
hypo- 
tonic, or 
atonic,  or 
atrophic 
paralysis 
(472). 
(Figs  24-6) 


paralysis  in  which  the  muscles  have  lost 
their  tone  and  offer  little  or  no  resist- 
ance to  passive  motion,  even  when 
rapid.  The  joint  has  a  normal  or  even 
increased  excursion.  The  muscles  ex- 
hibit a  great  and  rapid  atrophy,  and 
under  the  microscope  their  fibers  show 
a  loss  of  their  transverse  striation  and 
various  forms  of  degeneration  (fatty, 
hyaline,  etc.).  The  electrical  reaction 
of  degeneration  is  present  (399).  When 
muscles  are  completely  degenerated 
(404)  passive  contractures  (263)  may 
occur.  The  tendon  reflexes  are  abol- 
ished or  diminished. 


Destructive  lesion  of  peripheral 
motor  neurons  (462).  It  oc- 
curs in  diseases  of  the  mus- 
cles, peripheral  nerves,  ante- 
rior horns  of  cord,  or  motor 
nuclei  in  brain  stem.  It  is 
never  functional,  but  may  be 
somewhat  simulated  by  joint 
disease.  Hypotonia  without 
muscular  paralysis  or  atrophy 
occurs  in  cerebellar  lesions, 
tabes  and  other  ataxic  con- 
ditions (240). 


253  A  rapid  tiring  of  muscles  upon  exercise.     A 

Myasthenic      myasthenic    reaction   to   electricity    (401). 

paralysis      Muscles   show    small    foci  of  small  round 

(553)  cells. 


A  lesion  of  the  muscles  and 
often  of  thymus  gland. 


MOTOR  PARALYSIS     (Continued) 
Diagnostic 
Symptoms  Definition 

f  254  A  paralysis  with  exaggerated  tendon  reflexes, 

Hemiplegia      of  one  lateral  half  of  the  body  and  extremi- 
(478-9)         ties  limited  by  the  median  line  in  front  and 

(Figs.  17-24)  behind.  It  is  partial,  if  limited  to  arm  and 
leg;  complete,  if  arm,  leg,  tongue,  palate  and 
face  are  all  involved.  In  some  cases  of  hemi- 
plegia there  are  slight  weakness  and  exagger- 
ated reflexes  on  the  other  side  of  the  body 
also,  especially  in  the  leg.  Symmetrical,  bi- 
lateral muscles,  which  have  a  common  func- 
tion and  a  bilateral  cortical  innervation,  arc 
not  paralysed;  at  most  temporarily  weak- 
ened. Such  are  the  ocular,  masticatory, 
laryngeal,  respiratory,  bladder,  rectal,  etc., 
muscles.  In  cerebral  hemiplegia  certain 
muscles  are,  in  most  cases,  more  completely 
paralysed  than  others.  These  "predilection 
muscles  of  Wernicke"  are  the  trapezius,  the 
external  rotators  and  adductors  of  the  upper 
arm,  the  triceps,  the  supinators  and  abduc- 
tors of  thumb,  the  extensors  of  the  thigh, 
the  flexors  of  the  leg  and  the  dorsal  flexors 
of  the  foot. 

255  A   double    hemiplegia    involving    both   sides. 

Diplegia  May  be  complete  or  partial  and  not  infre- 

(478)  quently  is  limited  to  the  legs,  or  the  face 

(facial  diplegia),  etc. 


Significance 
A  lesion  of  the  contralat- 
eral central  motor  neu- 
rons (461).  In  extremely 
rare  cases  the  lesion  may 
be  homolateral  (homo- 
lateral hemiplegia),  in 
which  cases  the  pyra- 
midal tract  may  not 
decussate  in  the  med- 
ulla. Hemiplegia  is  usu- 
ally due  to  a  cerebral 
lesion,  but  the  partial 
form  may  be  due  to  a 
bulbar  or  spinal  lesion, 
very  rarely.  Very  rarely, 
there  may  be  no  lesion, 
except  an  extreme  local 
anemia  or  edema  of  brain 
as  in  nephritis  (hemiple- 
gia sine  materia). 


A  lesion,  usually  but  not 
always  cortical,  of  the 
central  motor  neurons  or 
basal  nuclei  on  both  sides. 


256  A  paralysis    of 

Crossed  one   or    more 

paralysis  homolateral 

(537-42)  cranial  nerves 

(Hemiplegia  and  of  the 

alternans)  contralateral 

(Figs.  20-1)  arm  and  leg. 


Always  due  to  a  lesion  involving  the  pyramidal  tract 
with  other  structures  in  the  brain  stem  (460) ;  either  in 
the  medulla  (hypoglossal  hemiplegia  alternans  (1268)), 
the  pons  (facial  hemiplegia  alternans  (1269)),  or  in  the 
cms  cerebri  (motor  oculi  hemiplegia  alternans  (1270)). 
The  nuclei,  or  the  neurons,  peripheral  or  central,  of 
the  cranial  nerves  are  involved  below  the  decussation 
of  their  central  neurons. 


257  A  symmetrical  par- 

1'araplegia       alysis      of      both 
(480)  sides  of  the  body. 

(Figs.  24-6)  Usually  only  in- 
volves the  legs  and 
lower  pari  of  bod] . 

lint  may  involve 
the  arms  and  even 
both  sides  of  the 
face. 


May  occur  in  lesions  of  the  muscles  (dystrophies) 
(477),  or  of  the  peripheral  nerves  (neuritis  (488- 
9)),  or  of  the  spinal  cord  or  brain  stem,  or  even 
of  the  cerebral  cortex  (bilateral  lesion).  The 
distinction  between  paraplegia  and  diplegia  (255) 
is  not  always  sharply  drawn.  In  general  diplegia 
is  applied  to  paralyses  of  cerebral  origin,  para- 
plegia to  those  of  spinal  or  peripheral  origin. 


2">s  A   paralysis  of  one  ex- 

Monoplegia       t  remit  y  only,  Or  of  one 


i  179 
(Fig.  15) 
200 

Local 

paralysis 

i  Mi 

(Fig.  16) 
200 

Aphonia 

(787  B) 


half  of  the  face  only, 


\la\    be  due  to  lesion  of  motor  cerebral  i 

Or  of  the   motor  nuclei,   or  of  the   peripheral 

nerves. 


A  paralysis  limited  to  one  or  more 
muscles  of  the  face,  eye,  mouth, 
neck,  bod]   or  extremitic       I  i 

than  a  whole  extremity. 


May  be  due  to  lesions  of  muscles  or 
of  peripheral  net  vm,  or  of  spinal 
cord,  or  rarely  of  motor  cerebral 
cortex,  or  functional 


Inability  to  produce  vocal 
sound-  Absence  of  voice, 
but  whispering  is  pos- 
sible. 


A  \  ariety  of  local 

pai  alysis. 


Laryngeal   paralysis,  o;- 

ganio  Or  functional. 


Methods  tor  the  detection  of  paralysis  and  paresi  bedinCharl  I  b. 

For  further  consideration  of  these  symptoms  and  of  the  diseases  in  which  th 

X. 

r.7 


CHART  IV  b 

Spasm 

Comprising  Numbers  245  to  247  and  263  to  276 


O'.i 


ANALYSIS  OF  THE  OBJECTIVE  SYMPTOMS  OF  THE  CASE  (SEMEIOLOGY) 


SPASM 


Diagnostic 
Symptoms 


Definition 


245 
T 
O 
N 
I 
C 

S 
P 
A 
S 
M 


'  263  A  continuous  contraction  of  long  duration  in  which 

Passive  the  muscles,  tendons  and  ligaments    have  be- 

contrac-       come  anatomically  shortened  and  cannot  be  ex- 
ture  tended  by  force,  even  under  etherization.     The 

(Figs.  24-6)  muscle  fibers  are  degenerated,  while  the  connec- 
tive tissue  of  the  muscle  is  hypertrophied  and 
usually  secondarily  contracted,  as  in  other 
newly  formed  connective,  or  scar,  tissue. 


264  A  continuous  contraction  lasting  weeks,  months, 

Active  or  years,  which  can  be  overcome  by  force,  either 

contrac-       with  or  without  etherization.    Muscles  are  in  a 

ture  normal  condition  of  nutrition.    Most  common  in 

(Figs.   15,       the  arms,  or  legs,  or  neck  muscles  (torticollis). 

17,  24-6)     The  active  contracture  of  a  hemiplegia  is  usually 

that  of  flexion  in  the  arm  and  of  extension  in 

the  leg. 


265  An  active  contracture  of  brief  duration  but  much 

Myotonia         longer  than  a  convulsive  tic.    It  may  occur  at 
(613)  the  commencement  of  voluntary  motion  (Thorn- 

sen's  disease,  or  myotonia  congenita)  or  may  be 
excited  by  cold  (Eulenberg's  disease,  or  para- 
myotonia congenita).  It  is  frequent  in  menin- 
gitis and  tetanus  in  which  it  takes  many  forms, 
viz:  "retraction  of  head;"  "trismus,"  strong 
closure  of  jaw;  "  opisthotonus,"  arching  of  body 
backwards;  "  pleurosthotonus,"  bending  of  body 
to  one  side;  "  emprosthotonus,"  arching  0f 
body  forwards  and  "  orthotonus,"  holding  0f 
body  rigid  and  straight. 


266  An  active  contracture  of  such  mild  degree  that  it 

Rigidity  does   not   prevent  passive,  or  even  voluntary, 

motion  of  the  part,  although  rendering  it  diffi- 
cult (paralysis  agitans  (612)),  etc. 


267  A  violent  spasm  of  momentary  duration.  If  rapidly 

Convulsive      repeated  it  must  be  classed  under  myoclonus 

tics  (270  and  601-4).     If  painful    it  is  called  '   tic 

(601)  douloureux  "  (602). 


268 
Reflex 

spasm 


A  spasm,  usually  tonic,  caused  by  irritation  of 
some  sensory  tissue. 


Significance 
Due  to  muscular  lesions  and 
to    degeneration    of    the 
peripheral  motor  neurons 

(462). 


Active  contractures  occur- 
ring in  hemiplegia  affect 
the  muscles  not  abso- 
lutely paralyzed.  When 
the  contracture  is  over- 
come by  the  application 
of  a  plaster  of  Paris 
splint,  the  muscles  often 
show  a  surprising  degree 
of  voluntary  motion, 
when  the  splint  is  re- 
moved. These  contrac- 
tures depend  in  part,  on 
attempts  at  voluntary 
movements  and  on  asso- 
ciated movements,  but 
n  greater  part  on  reflex 
action  from  sensory  irri- 
tation ;  the  inhibitory  ac- 
tion of  the  brain  being- 
cut  off  by  the  lesion. 
They  never  occur  in  hem- 
iplegia in  tabetics  and 
in  any  case  can  be  re- 
lieved by  section  of  the 
posterior  nerve  roots. 
Such  contractures  are 
always  of  very  bad  prog- 
nosis as  to  recovery. 

Active  contracture  is  some- 
times due  to  paralysis  of 
antagonist  muscles  or  to 
muscle  lesions. 

All  tonic  spasms  (not  in- 
cluding passive  contrac- 
ture) are  due  to  a  func- 
tional disorder,  or  are  re- 
flex (especially  in  chil- 
dren), or  are  due  to  irrita- 
tion (chemical,  sensory  or 
vascular)  of  central 
motor  neurons  (461). 
Painful  cramps,  espe- 
cially in  legs,  of  the  na- 
ture of  myotonia  or  tics, 
may  be  due  to  a  defi- 
ciency of  water  in  the 
system. 


70 


Diagnostic 
Symptoms 


SPASM  (Continued) 


Definition 


246 
C 


247 
I 

R 
R 
E 
G 
U 
L 
A 
R 

S 
P 
A 
S 
M 
S 


269  Violent  clonic  contractions  of  many,  or  of  all  the, 
Convulsion      muscles  of  the  body. 

(571) 

270  Successive  clonic  contractions  of  one,  or  of  a  few 
Myoclonus       adjacent    muscles.       Repeated    convulsive    tie. 

or  Most  common  in  the  face  muscles   (blepharo- 

convul-        spasm  (601)). 
sive  tics 

'271  Slow,  worm-like,  rhythmical  movements,  often  " 

Athetosis         associated     with      transitory      contractures 

or  mobile     (spasmus  mobilis),  of  fingers  and  wrists  and 

spasm  more  rarely  of  toes  and  ankles.      Hyperex- 

(574)  tension  is  the  predominant  action.     Usually 

unilateral,    but    may    be    bilateral.       Much 

more  common  in  children  than  in  adults. 

Muscles  of  the  neck,  face  and  of  other  parts 

of  the  body  are  not  infrequently  involved. 

272  Rapid,  irregular,  co-ordinated,  but  purposeless 

Choreic  movements  caused  by  contraction  now  of  one 

move-  group  of  muscles,  now  of  another,  throughout 

ments  the  body;  bilateral  or  unilateral  (hemichorea). 

Chorea  minor  Cease  during  sleep.    They  often  render  volun- 
(573)  tary  movements  ataxic  and  are  usually  asso- 

ciated with  a  mild  degree  of  paralysis  of  the 
muscles  involved. 


Patient  performs  involuntarily  and  uncontrol- 
ably  a  complicated  and  apparently  purposeful 
movement.  Also  applied  to  a  coarse  tremor  or 
violent  oscillation  of  a  part  of  the  body. 

Patient  frequently  performs  involuntarily,  and 
usually  unconsciously,  the  same  act.  Usually 
a  small  act. 


273 
Chorea 

major  or 

magna 

(628) 
274 
Habit 

chorea 

(626) 

275  Patient  is  compelled  hy  some  power  within  him 
Compulsory    which  he  cannot  understand  or  explain   to 

acts  (218)     perform  certain  acts  against  his  will. 

276  Muscular  contractions, occurring  when  movements 
Associated      are  executed  <>r  attempted,  in  muscles  not  di- 

move-  rectlv  concerned  in  the  movement   attempted; 

ments  often  the  corresponding  muscles  of  the  opposite 

side  of  the  body,  often  those  of  the  face.  Such 
associated  movements  are  Hell's  phenomenon 
i  III      Strumpell's    tibialis    phenomenon      ill.".-, 

lialnnski's  associated  movements  in  unilateral 
paralysis  (•(  16). 


Significance 

Clonic  spasms  are  usually 
due  to  irritation  of  the 
cerebral  cortex,  but  may 
also  result  from  very  exag- 
gerated reflexes  (clonus). 


Lesion  is  usually  in  pos- 
terior part  of  optic  thal- 
amus or  corpus  striatum 
of  contralateral  hemi- 
sphere and  not  causing 
complete  paralysis.  Le- 
sion may  involve  the 
fibers  connecting  the 
optic  thalamus  with  the 
cerebral  cortex.  May  oc- 
cur in  diffuse  cortical 
lesions. 


Functional  disorders,  occur- 
ing  in  the  neuroses  and 
in  insanitv. 


In  such  cases  movements 
often  associated  together, 
but    which  can  be  easily 

dissociated  voluntarily  in 

health,  cannot  he  disso- 
ciated in  disease  which 
cuts  off  voluntarv  action. 


Methods  of  detection  of  spasm  are  described  m  ('hart    I  b. 

For   further  discussion    of   these   symptoms,   and    of   the   diseases   in    which    they   occur.   BOS 
Charts   XI   and   XII. 


71 


CHART  IV  c 

Perversions  of  Motion 
Ataxia,  Loss  of  Skill,  Tremor 

Comprising  Numbers  248  to  250  and  280  to  293 


73 


ANALYSIS  OF  THE  OBJECTIVE  SYMPTOMS  OF  THE  CASE  (SEMEIOLOGY) 
ATAXIA— LOSS  OF  SKILL 


Diagnostic 
Symptoms 
280 
Motor 

ataxia 

(644) 

(dynamic 

ataxia) 
(Figs.  24-6) 


Definition 
Voluntary  movements  are  executed  in 
an  irregular  and  disorderly  manner, 
which  is  due  to  a  loss  of  the  co-ordi- 
nating power.  Rarely  associated 
with  decided  vertigo. 


2S1  Walking  and  standing  are  inco-ordi- 

Cerebellar        nate,  but  other  acts  are  not,  or  only 

ataxia  slightly  so.    Patient  executes  simple 

(642)  movements   of  his   legs   fairly   well 

(static  when  lying  in  bed,  but  in  walking 

ataxia)         and  standing  he  lacks  synergy  of  the 

(Figs.  19-26)  muscles  and  staggers  and  sways  like 

a  drunken  man.    Usually  associated 

with  vertigo  (392). 


282  Inability,  or  difficulty,  in  performing 

Apraxia  a  desired  and  accustomed  act  because 

(Fig.  15)      of    loss,  or    derangement,     of    the 

innervation  memories  concerned  in 

that  act.     Loss  of  skill. 


Significance 
Is  due  to  a  loss  of  muscle  sense  (42) 
(deep  sensibility).  May  be  due  to 
lesions  of  peripheral  sensory  nerves, 
or  of  posterior  columns  of  cord,  or  of 
brain  stem,  or  of  cerebral  cortex 
posterior  to  fissure  of  Rolando,  or 
may  be  toxic  (alcohol),  or  functional. 

Is  due  to  a  lack  of  muscular  synergy 
(41)  (asynergy).  Due  to  lesion  or 
functional  disorder  of  the  cerebellum 
or  its  tracts,  including  the  direct 
cerebellar  tract  in  brain  stem  or 
cord,  or  to  tumors  in  frontal  lobe  of 
brain,  or  to  disease  of  ears  or  eyes, 
or  to  poisons  (alcohol,  etc.).  In 
lesions  of  the  cerebellar  hemisphere 
the  disorder  is  transitory;  in  lesions 
of  the  worm  it  is  more  permanent. 

Loss  of  innervation  memories,  general 
or  partial,  due  to  cortical  or  sub- 
cortical lesions  (anterior  or  posterior 
central,  or  supra-marginal  convolu- 
tion) or  to  functional  or  anemic 
disorders  of  cerebral  cortex.  (See 
page  26-7). 

May  be  either  functional  or  organic 
and,  if  the  latter,  may  or  may  not 
be  due  to  lesions  in  the  organs  of 
speech.  If  not,  it  is  called  pure 
motor  aphasia  or  aphemia. 


283  Absence  of  speech.   Speech  may  never 
Anarthria        have  been  acquired,  as  in  idiocy,  or 

(737)  it  may  be  voluntarily  restrained  for 
a  purpose;  or  it  may  be  more  or 
less  involuntarily  restrained,  as  in 
insanity  or  hysteria. 

284  Such    difficulty    in    articulation    that 
Dysarthria      speech     becomes     indistinct     and 

(738)  blurred,  but  is  probably  never  so 
great  as  to  cause  complete  anarthria 
(283). 

285  Difficulty  in  swallowing. 
Dysphagia 

286  Difficulty  in  mastication. 
Dvsmasesis 

(553) 

287  Complete  inability  to  stand  or  walk 
Astasia  and     but  legs  can  be  moved  freely,  even 

Abasia         strongly,  when  lying  or  sitting. 
(653  and  792) 

288  Difficulty    in    repeating   a    movement     Occurs  in  lesions  of  a  cerebellar  hem- 
Diadocoki-      rapidly,  especially  supination.  isphere,  or  is  functional. 

nesia  (36) 

74 


Occur  in  lesions  of  the  medulla  and 
pons  (bulbar  paralysis,  Figs.  21-3) 
and  of  the  cranial  nerves.  Also  in 
diphtheria,  hydrophobia,  myasthe- 
nia gravis,  rarely  in  trichinosis 
and  frequently  in  hysteria  (globus 
hystericus). 


A  delusion  or  auto-suggestion,  which 
occurs  in  hysteria.  May  occur  rarely 
in  cerebellar  lesions. 


250 
T 
R 
E 
M 
O 
R 


TREMOR 

Diagnostic 

Symptoms  Definition 

289  Involuntary,  rhythmical  oscillation  or 

Passive  trembling  of  a  part  which  is  other- 

tremor         wise  at  rest. 

(646  and  647) 


290 

Intention 

tremor 

(64.5) 

291 
Nystagmus 

'(640) 


An  involuntary  tremor  which  only 
occurs  when  a  voluntary  motion  is 
made,  or  is  willed  and  is  about  to 
be  made. 


An  involuntary  trembling  or  oscillation  of 
eyeball,  usually  horizontal,  rarely  verti- 
cal, very  rarely  rotatory.  Increased,  or 
only  occurs,  on  voluntary  motion  of  eyeball, 
especially  on  extreme  deviation.  The  rapid- 
ity of  the  oscillations  varies  from  60  to  200 
per  minute.  Their  amplitude  from  2  to  4 
millimeters.  Nystagmus  may  be  oscillatory 
when  the  motion  in  each  direction  is  equally 
rapid,  or  rhythmic  when  it  is  quicker  in  one 
direction  than  in  the  other. 


Significance 
Functional.      Occurs  in  paralysis  ti- 
tans, weakness,  etc. 


Functional  and  organic.  Occurs  in 
neuroses  and  in  organic  diseases 
(disseminated  sclerosis) 


Occurs  especially  in  lesions  of 
the  vestibular  and  other  nuclei 
in  the  pons,  Deitcr's  nucleus 
in  the  cerebellum,  the  pos- 
terior longitudinal  bundle  in 
the  brain  stem,  in  disturb- 
ances in  the  semi-circular 
canals,  and  in  weakness  of 
ocular  muscles,  and  in  lesion 
of  ponto-cerebellar  angle ; 
also  in  the  caloric  reaction 
(79),  and  in  cerebellar  disease 
(80). 


292 


An  involuntary  contraction  of  a  bundle 


I  ibrillary  of  fibers  of  a  muscle  of  short  dura- 
contrac-  tion.  When  many  occur  in  adjacent 
tion  or  bundles  at  short  intervals,  waves  of 
fibrillation  contraction  run  over  the  muscle,  but 
(641)  do   not   cause   it   to  contract   as   a 

whole. 


293 
Myokymia 


A  fibrillary  twitching  of  the  muscles 

occurring  in  healthy  persons. 


Degeneration  of  those  multipolar  nerve 
cells  in  the  anterior  horns  of  the 
spinal  cord  and  brain  stem  of  which 
the  motor  nerves  supplying  the  mus- 
cle are  the  axons.  Rarely  occurs  in 
traumatic  neuroses. 


Normal.  Exhaustion.  Following  ex- 
cessive muscular  contraction  or  ex- 
posure to  cold. 


Method-  of  detection  of  perversions  of  motion  are  described  in  ('hart  I  b. 

For  the  further  discussion  of  these  symptoms  and  of  the  diseases   in    which   thev   0CCU1 
Chart    XII. 


78 


CHART  V 

Reflex  Activity 


ANALYSIS  OF  THE  OBJECTIVE  SYMPTOMS  OF  THE  CASE  (SEMEIOLOGY) 
Definition,  Significance  and  Relationship  of  the  symptoms  of  disease. 

f297  CUTANEOUS  OR  SUPER- 
FICIAL REFLEXES 
A  reflex  act  which  originates  from 
an  irritation  of  the  skin  (57). 


296  REFLEX  ACTS 

An  involuntary  movement  caused 
by  irritation  of  a  sensory  nerve 
or  terminal  organ.  Although 
not  the  result  of  conscious  in- 
tention, yet  these  acts  seem  pur- 
poseful and  usually  tend  towards 
the  protection  of  the  body.  In 
order  that  a  reflex  act  may  take 
place  there  must  be  a  compara- 
tively healthy  reflex  arc,  con- 
sisting of  a  motor  nerve,  a  sen- 
sory nerve  and  some  gray  mat-- 
ter  connecting  the  two;  or,  in 
other  words,  :i  motor  neuron 
and  a  sensory  neuron  connected 
together  directly  or  by  a  bridg- 
i ri ti  neuron.  Keflex  acts  are  in- 
hibited and  modified  by  inhib- 
itory impulses  passing  down 
from  the  brain  along  the  so- 
called  inhibitory  filler.--,  which 
are  also  the  central  motor  neu- 
rons (the  pyramidal  tract)  (472- 
4,  810).     (Figs.  19,  24). 


298  MUCOUS  MEMBRANE 
REFLEXES 

A  reflex  act  which  originates  from 
an  irritation  of  a  mucous  mem- 
brane (58). 


299  TENDON  OR  DEEP 
REFLEXES 

A  reflex  act  which  originates  from 
the  sudden  stretching  of  the 
fibers  of  a  muscle  (60-6). 


300  ORGANIC  REFLEXES 

A  reflex  act  affecting  one  of  the 

viscera  of  the  body  (1),  especially 

the  bladder  or  n  ctum. 


301  VASO-MOTOR   IM  II  I  \l  s 

A  reflex  act  affecting  the  arterioles 
(59). 


302  PUPILLARY  EU  I  LEX 

A   reflex  act   affecting  the  pupil 
(25-7). 


The  conditions  in  which 
reflex  acts  are  disor- 
ordered  are  set  forth 
in  Chart  Y  a. 


The  conditions  in   which 

the   pupillary    n 

arc    disordered    I 
forth  in  Chart  V  b. 


:: 


CHART  V  a 

Cutaneous  or  Superficial  Reflexes,  Mucous  Membrane 

Reflexes,  Tendon  or  Deep  Reflexes,  Organic 

Reflexes,  Vaso-Motor  Reflexes 

Comprising  Numbers  303  to  326 


7'.. 


ANALYSIS  OF  THE  OBJECTIVE  SYMPTOMS  OF  THE  CASE  (SEMEIOLOGY) 
CUTANEOUS  REFLEXES 


Diagnostic       Definition  and  Location  of 
Symptoms  Reflex  Centers 

303  Plantar  flexion  of  the  toes  when 
Plantar  the  sole  of  the  foot  is  irritated. 

(1st  and  2nd  sacral  segments.) 

304  Sluggish    extensive  dorsal  flexion 
Babinski's  of  the  great  toe  when  the  sole  of 

the  foot  is  irritated. 

305  Dorsal    flexion    of   the  great  toe 
Gordon's  when    deep    pressure    is    made 

through  the  calf  muscle  on  the 
deep  flexor  muscles  beneath ;  the 
leg  being  completely  relaxed. 

306  Dorsal    flexion    of    the  great  toe 
Oppenheim's       elicited  by  firm  stroking  with  a 

hard  object,  or  finger,  just  be- 
hind the  postero-internal  border 
of  the  tibia  from  above  down- 
wards ;  the  leg  being  completely 
relaxed. 


307 
Gluteal 


307a 
Anal 


Contraction  of  the  buttocks  when 
the  skin  covering  them  is  irri- 
tated. 

(4th  and  5th  lumbar  segments.) 

Contraction  of  sphincter  ani  upon 

pin  pricks  of  anus. 
(5th  sacral  segment.) 


308  Drawing  up  of  the  testicle  when 
Cremasteric         the  inner  side  of  the  thigh  is 

irritated. 
(1st  to  3rd  lumbar  segments.) 

309  Sudden  movement    of    umbilicus 
Umbilical  towards   the   side   of   abdomen 

irritated. 
(8th  to  12th  dorsal  segments.) 

310  Sudden  retraction  of  epigastrium 
Epigastric  when    the    hypochondrium    is 

irritated. 
(7th  to  9th  dorsal  segments.) 

311  Drawing   inwards   of  the  scapula 
Interscapular      when  the  skin  of  the  interscap- 
ular space  is  irritated. 

(5th   cervical   to    1st   dorsal   seg- 
ments.) 

312  Closing   of  the   eyelids  when    the 
Corneal  or  cornea    or    conjunctiva    is    irri- 

conjunctival    tated. 

(5th  to  7th  cranial  nuclei.) 

313  Sneezing    when    the    nasal    mem- 
Nasal  brane  is  irritated. 

(5th   to    10th    cranial    and    upper 
cervical  nuclei.) 


Significance 
The  abnormal  reflexes,  Babinski,  Gordon  and 
Oppenheim  reflexes  and  ankle-clonus,  always 
indicate  disease  of  the  central  motor  neurons 
(461),  except  in  infants,  in  whom  these  re- 
flexes (except  ankle-clonus)  may  be  present 
normally,  and  in  some  cases  of  hysteria  in 
which  an  imperfect  ankle-clonus  may  rarely 
be  obtained.  The  Babinski  reflex  is  most  re- 
liable in  a  diagnostic  sense.  The  Oppenheim 
reflex  is  sometimes  present  when  the  Bab- 
inski is  absent  and  vice  versa.  Kernig's  sign 
indicates  meningitis  or  meningismus;  it  is  an 
important,  but  not  a  certain,  diagnostic  sign. 

Alterations  in  the  tendon  reflexes  are  of  very 
much  greater  diagnostic  value  than  are  those 
of  the  cutaneous  (except  the  Babinski)  re- 
flexes, which  are  in  many  cases  inconstant, 
probably  because  the  cutaneous  reflex  im- 
pulses may  even  pass  through  the  gray  matter 
of  the  brain  (cerebellum)  as  well  as  through  a 
wide  area  of  that  of  the  spinal  cord. 

Diminution  of  reflexes  is  usually  of  little  diag- 
nostic value,  but  their  abolition  is  of  great 
value  and  maybe  due  to  a  destructive  lesion  of 
any  part  of  the  reflex  arc  (a  peripheral  motor 
neuron,  a  peripheral  sensory  neuron,  or  a 
central  bridging  neuron).  When  there  is  a 
lesion  of  the  peripheral  motor  neuron,  atro- 
phic motor  paralysis  is  present  in  addition 
to  the  loss  of  the  reflex.  When  there  is  a 
lesion  of  the  peripheral  sensory  neuron  there 
is  usually  a  sensory  paralysis  (anesthesia, 
etc.),  in  addition  to  the  loss  of  the  reflex. 
Diminution  or  abolition  of  reflex  activity 
(cutaneous  or  tendon)  may  occur,  at  least 
temporarily,  in  acute  diseases  or  other 
forms  of  irritation  of  the  central  motor 
neurons;  also  in  cases  of  shock,  exhaustion, 
coma,  narcotism  and  after  epileptic  fits, 
(except  Babinski);  also  by  will  power 
and  by  voluntary  movements  of  the  muscles 
concerned;  also  (except  Babinski)  in  cases 
of  complete  separation  of  the  brain  from  the 
spinal  cord,  and,  rarely,  of  increased  intra- 
cranial pressure,  also  frequently  in  fevers. 

The  abolition  of  the  knee-jerk  is  of  great  diag- 
nostic importance.  It  is  absent  in  tabes, 
neuritis  (multiple  and  crural),  acute  anterior 
poliomyelitis  involving  the  extensor  cruris, 
Landry's  paralysis,  lesion  of  the  cauda  equina 
or  of  the  lumbar  enlargement,  during  the 
attack  of  family  periodic  paralysis,  when 
exhausted  after  an  epileptic  attack  and  in 
cases  of  muscular  dystrophy  involving  the 
extensor  cruris  muscles.  It  is  usually  abol- 
ished in  Friedreich's  ataxia  and  combined 
sclerosis  except  in  the  early  stages  when  it 
may  be  increased.  It  may  be  absent  in 
cerebral  compression  (tumor  or  meningitis) 
and  in  some  cases  of  cerebellar  disease,  and 
may  then  be  unilateral.  It  may  be  absent 
also  in  the  conditions  mentioned  in  the 
preceding  paragraph. 


80 


MUCOUS  MEMBRANE.  TENDON,  ORGANIC  AND  VASO-MOTOR  REFLEXES 


Diagnostic 
Symptoms 
314 
Uvular 


315 
Pharyngeal 

316 

Ankle-clonus 


317 

Achilles 
reflex 

318 
Knee-jerk 


319 
Kernig's  sign 

320 

Dorsal  foot 
reflex 


Definition  and  Location  of 
Reflex  Centers 
Raising  of  the  uvula  in  phonation 

or  upon  irritation  of  its  mucous 

membrane. 
(9th  to  10th  cranial  nuclei.) 

Retching    or    gagging    when    the 

pharynx  is  irritated. 
(9th  to  10th  cranial  nuclei.) 

Oscillation  of  the  foot  when  the 
ball  of  foot  is  pressed  quick- 
ly and  continuously  upwards. 

(5th  lumbar  and  1st  sacral  seg- 
ments.) 

Sudden  plantar  flexion  of  foot 
when  the  tendo  -  Achillis  is 
sharply  struck. 

(1st  to  2nd  sacral  segments.) 

Sudden  extension  of  knee  when  the 
ugamentum  patellae  is  sharply 
struck.  When  this  reflex  is  ex- 
aggerated it  is  usually  accom- 
panied by  a  contraction  of  the 
adductors  of  the  opposite  thigh, 
or  even  by  knee  clonus  (61). 

(2nd  to  4th  lumbar  segments.) 

Resistance  to  sudden  extension  of 
the  knee. 

Sudden  plantar  flexion  of  the  toes 
when  the  dorsum  of  the  foot 
over  the  4th  and  5th  metatarsal 
bones  is  struck. 

(5th  lumbar  and  1st  sacral  seg- 
ments. | 

Sudden  extension  or  flexion  of  el- 
bow or  wrist  when  the  corres- 
ponding tendons  are  sharply 
struck. 

(5th  to  7th  cervical  segments.) 

Sudden  closure  <>f  jaw  when  it  is 

sharply  struck  downwards. 
(61  ii  oranial  nucleus.) 

The  retention  of  mine  in  the  blad- 
der by  the  sphincter  reflex,  and 

i  (pulsion  of  urine  by  tin-  de- 
trusor reflex  and  the  synchro- 
nous relaxation  of  the  sphincter. 

(Hypogastric  sympathetic  ganglia.) 

Similar  to  that  of  the  bladder, 
orrhoidal  sympathetic 

lia.) 

den  pallor  of  the  skin  follow- 
ing an  irritation  and  limited  to 

the  area  of  irritation. 


Significance 
Exaggeration  of  the  reflexes  may  be  due  to  a 
mild  inflammation,  or  to  any  irritation,  of 
any  part  of  the  reflex  arc.  Strychnine  in- 
creases reflex  activity  by  irritating  the  nerve 
cells  in  the  anterior  horns.  More  commonly 
the  reflexes  are  increased  by  any  lesion  of 
the  motor  central  neurons,  thus  cutting  off 
the  normal  inhibitory  influence  of  the  brain, 
and  are  then  associated  with  paralysis  of 
voluntary  motion.  The  presence  of  ankle- 
clonus,  the  Babinski  reflex  and  the  dorsal 
foot  reflex  indicates  a  lesion  of  the  pyramidal 
tract  much  more  certainly  than  does  an  ex- 
aggerated knee-jerk,  unless  the  latter  is 
associated  with  an  adductor  contraction. 
Very  commonly  the  reflexes  are  increased 
in  functional  diseases  (hysteria)  and  in 
nervousness. 


Innervation  of  the  muscles  not  concerned  in 
the  reflex  act  and  diverting  the  attention 
increases  reflex  activity  (reinforcement,  68). 


The  paradoxical  reflex  is  of  no  diagnostic  im- 
portance. It  consists  in  a  contraction  of  the 
tibialis  instead  of  the  calf  muscles  when 
ankle-clonus  is  tested  for;  also  of  a  con- 
traction of  the  flexors  instead  of  the  exten- 
sors of  the  thigh  when  the  knee-jerk  is 
tested  for. 

In  the  dorsal  foot-rellex  i  Mendel-Bechterewt 
normally  there  is  either  no  reflex  or  a  dorsal 
flexion  of  the  toes,  but  in  cases  of  pyramidal 
tract  lesions  a  plantar  flexion  of  the  toes 
occurs. 


321 
Elbow  and 

wrist 

reflexes 

322 
Maxillary 

rellex 

323 

Bladder  or 
vesical 

reft  x 

;!-'  I 

Rectal 

325 
Ischemic 

reflex 

326 
Para!' 
hyperemic  Congestion  <>f  the  skin  following 

p  fl(  \  the    ischemia    due   to   irritation  ; 

(dermogra-     (t&chee  oerebralea  and  dermo- 

phiai  graphia). 

The thoda  of  eliciting  'he  various  n  ed  in  Char)  1  o. 

isee  in  which  the  reflexes  are  altered  are  discussed  in  Charts  X.  \i\ 

81 


Inability  to  void  urine,  or  to  retain  it.  is  some- 
times  due   to  nervousness   and   sometimes   to 

mechanical  obstruction  (enlarged  pro-1 

stricture),  imt  any  other  serious  disturbance 

of  the  Organic  reflexes  indicates  organic  dis- 
ease of  t  he  nervous  system.  1 1  never  occurs  in 
diseases  limited  to  the  peripheral  nerves,  ex- 
o  pt  in  lesions  of  the  cauda  equina,  and  rarely 

in  cerebral  disease.      It    i-  most   common   in 

spina]  disease,  Bphincter  paralysis  with  empty 
bladder  and  constant  dribbling  of  urine  in 
ne  of  lumber  enlargement,  and  detrusor 
paralysis  with  distended  bladder  and  often 
with  dribbling  of  urine  in  lesions  above  the 
lumbar  enlargement.    (Fig.  28 


Vasomotor  disturbances  cause  a   disturbance 

of  the  nutrition   of  a    part.      Diseases   which 

re.Milt  from,  or  are  associated  with,  disturb- 
anoes   of   the   vaso-motor   reflexes   an 

1  in  Chart   \  \  II. 


XVI,  \  \  1 1 


CHART  V  b 

Pupillary  Reflexes 

Comprising  Numbers  302  and  330  to  341. 


83 


ANALYSIS  OF  THE  OBJECTIVE  SYMPTOMS  OF  THE  CASE  (SEMEIOLOGY) 


Diagnostic 
Symptoms 

330 

Pupillary 
reaction 
to  light 
(25) 


PUPILLARY  REFLEXES 
Definition  and 
Location  of 


Reflex  Centers 

Pupil  contracts  when 
light  is  thrown  on 
retina  of  the  same 
eye  (direct  reflex), 
and  when  light  is 
thrown  on  retina  of 
opposite  eye  (con- 
sensual reflex),  and 
dilates  when  retina 
is  shaded  from  light 
(ciliary  ganglion). 


331 

Pupillary 
reaction 
to  accom- 
modation 
(27) 


Pupil  dilates  when  pa- 
tient looks  at  a  dis- 
tant object  and  vis- 

■  ual  axes  are  parallel 
and  contracts  when 
patient  looks  at  a 
near  object  and  eyes 
converge. 


332 

Argyll- 
Robert- 
son's phe- 
nomenon 
(447,  891) 


Pupil  does  not  re- 
spond to  light,  but 
does  respond  to  ef- 
forts at  accommo- 
dation. 


333  The    pupil    responds 
Immobile         neither  to  light  nor 

pupil  accommodation,  but 

(545)  in  some  cases  may 

still  dilate  slightly 
on  irritation  of  cer- 
vical sympathetic. 

334  Pupil  contracts  when 
Hemiopic        light  is  thrown  on 

reflex  the      unparalysed 

(26)  half  of  retina,  but 

does  not  contract 
when  light  is 
thrown  on  para- 
lysed half. 


Significance 

The  pupillary  reaction  to  light  is  diminished  or  absent  in 
lesions  of  the  reflex  arc  (optic  nerve,  corpora  quadri- 
gemina,  the  Westphal-Edinger  cell  group  of  the  motor 
oculi  nucleus,  third  nerve  and  ciliary  ganglion),  espec- 
ially in  lesions  of  the  ciliary  ganglion.  When  the  op- 
tic nerve  or  corpora  quadrigemina  are  involved  the 
consensual  reflex  can  not  be  obtained  from  the  other 
(healthy)  eye.  It  is  absent  in  blindness,  deep  sleep, 
narcosis,  shock,  coma,  epileptic,  and  occasionally  in 
hysterical,  attacks;  also  absent  in  tabes,  in  many  cases 
of  paresis  and  in  rare  cases  of  syphilis  alone;  absent 
also  when  eye  is  under  the  influence  of  mydriatics  or 
myotics. 

The  pupillary  reaction  to  accommodation  is  absent  (cyclo- 
plegia)  in  lesions  of  the  third  nerve,  sometimes  after 
diphtheria,  occasionally  in  alcoholism  and  when  the 
eye  is  under  the  influence  of  mydriatics  or  myotics, 
also  in  myopia  and  in  cases  of  deficient  convergence. 

The  Argyll-Robertson's  phenomenon  occurs  in  almost  all 
cases  of  tabes  and  paresis  (in  many  of  these  cases  a 
degeneration  of  the  posterior  columns  of  the  cord  has 
been  found  at  autopsy)  and  very  rarely  in  cases  of 
syphilis  in  which  there  are  no  manifestations  of  either 
tabes  or  paresis  for  years  afterwards.  The  reverse  of 
the  Argyll-Robertson's  phenomenon,  i.e.,  the  preser- 
vation of  the  light  reflex  and  the  loss  of  the  accommo- 
dation reflex,  occurs  occasionally  in  diphtheritic  paral- 
ysis and  has  been  found  associated  with  syphilis,  basal 
meningitis,  tumors  of  corpora  quadrigemina  and  myelitis. 
It  is  extremely  rare. 

Immobile  pupil  may  occur  in  lesions  of  the  optic  nerve 
or  tract  or  in  its  nucleus  or  in  that  of  the  third  nerve 
or  in  the  ciliary  ganglion  or  its  nerve.  It  may  also  be 
associated  with  ophthalmoplegia  externa  or  interna  or 
both.  When  it  occurs  alone  it  is  due  to  a  lesion  in  the 
nucleus.  Immobile  pupil  also  occurs  in  tabes,  in  epi- 
lepsy, in  some  forms  of  hysteria,  in  fainting,  and  in 
katatonic  stupor. 

The  hemiopic  reflex  occurs  only  in  lesions  of  the  optic 
tract  or  geniculate  bodies  (homonymous  hemianopia) 
or  of  the  central  part  of  the  optic  chiasm  (bitemporal 
hemianopia).  The  existence  of  this  reflex  is  disputed 
by  many  observers. 


84 


PUPILLARY  REFLEXES     (Continued) 


Definition  and 
Diagnostic        Location  of 
Symptoms      Reflex  Centers 
335  Pupil     dilates     when 

Cilio-  neck  on  same  side 

spinal  is  irritated  or  when 

reflex  cocaine  is  dropped 

(465,  in  the  eye.     (Cer- 

1191—2)        vical     sympathetic 
ganglion.) 


336  When  the  eye  is  sud- 
Hippus  denly    exposed    to 

light,  there  occurs 
a  series  of  alternate 
contractions  and 
dilatations  of  the 
pupil,  gradually 
growing  less  in 
degree. 

337  When   patient's   eye- 
Westphal's      lids  are  held  fore- 
pupil  ibly  apart  and  he 
reaction       attempts    to    close 

them  he  not  only 
turns  the  eyeball 
upwards  (Bell's 
phenomenon)  but 
also  the  pupil  con- 
tracts. 

338  Pupil  dilates  instead 
Paradoxical     of  contracting  upon 

pupillary     exposure  to  light  or 


reflex 


upon  efforts  of  ac- 
commodation. 


339  Dilated  pupils. 
Mydriasis 

1 

340  Contracted  pupils. 
Myosit 


:*  II  One    pupil    is    largi  i 

Unequal  than  the  other  when 

pupils  t>r     the  eyes  are  al 

aniaoooria 


Significance 
The  cilio-spinal  pupillary  reflex  is  absent  in  lesions  of 
the  cervical  sympathetic,  and  in  many  lesions  of  the 
medulla  and  lower  cervical  and  upper  dorsal  region  of 
the  spinal  cord  (cilio-spinal  center — 465). 

Hippus  is  usually  associated  with  a  general  exaggeration 
of  reflexes. 

Westphal's  pupillary  reaction  occurs  in  some  cases  of 
tabes  and  in  paresis. 

The  paradoxical  pupillary  reflex  is  of  no  diagnostic  sig- 
nificance. It  has  been  observed  in  tabes  and  in  paresis 
and  is  the  result  of  fatigue. 

Mydriasis  may  be  irritative  or  spasmodic,  due  to  irrita- 
tion of  the  cervical  sympathetic  ganglion  or  nerve;  or 
may  be  paralytic,  due  to  paralysis  of  the  third  cranial 
nerve  or  the  ciliary  ganglion;  or  may  be  due  to  both 
causes.  It  occurs  in  children,  and  on  taking  certain 
drugs  (mydriatics).  It  occurs  also  from  irritation  of  the 
cervical  sympathetic  directly  by  incipient  lesions  in  the 
cervical  enlargement  of  the  spinal  cord  and  its  mem- 
branes, or  by  tumors  in  the  neck,  or  by  excess  of  car- 
bonic acid  in  the  blood  as  in  dyspnoea;  and  indirectly 
by  strong  emotions  and  especially  by  pain ;  also  in  par- 
alysis of  the  sphincter  pupillae  (iridoplegia)  from  le- 
sions, such  as  optic  atrophy,  glaucoma,  lesions  of  the 
third  nerve,  or  ciliary  ganglion,  which  break,  or  im- 
pair, the  reflex  arc,  and  which  usually  cause  more  or 
less  diminution  of  vision  and  a  deficient  perception  of 
light;  also  in  coma,  in  cases  of  increased  intra-cranial 
pressure,  and  in  some  other  cerebral  and  meningeal 
lesions  [especially  in  their  later  stages. 

Myosis  may  be  irritative  or  spasmodic,  due  to  irritation 
of  the  third  nerve  or  ciliary  ganglion;  or  may  be  para- 
lytic, due  to  paralysis  of  the  cervical  sympathetic  gang- 
lion or  nerve,  or  may  lie  ilue  to  both  causes.  It  occurs 
in  old  age,  in  deep  sleep,  or  on  taking  certain  drugs 
(myotics);  also  from  irritation  of  the  third  nucleus  or 
nerve,  as  in  meningitis  in  early  stages  and  especially 
in  hemorrhage  into  the  pons:  and  from  excessive  use  of 

accommodation,  as  in  watchmakers,  etc.;  also  from 
paralysis  of  the  sympathetic  in  lesions  of  the  neck  ami 
of  the  spinal  cord  (syringomyelia).  It  occurs  often  in 
tabes,  paresis,  iritis,  irritation  of  cornea  and,  tempor- 
arily, after  excision  of  the    Gasserian   ganglion. 

Aniscoria  occurs  in  many  conditions  and  is  of  little 
or  no  diagnostic  value. 


The  methods  of  eliciting  the  pupillary  reflexes  are  deseribed  in  Charj  I  b 

Diseases  in  which  these  reflexes  are  altered  are  discussed  in  Chart    X  I  V 


85 


CHART  VI 

Disorders  of  Sensation 


ANALYSIS  OF  THE  OBJECTIVE  SYMPTOMS  OF  THE  CASE  (SEMEIOLOGY) 
Definition,  Significance  and  Relationship  of  the  Symptoms  of  Disease. 


344  DISORDERS  OF  SENSA- 
TION 

The  power  of  receiving  perceptions 
of  the  external  world  and  of  the 
occurrences  in  our  own  body 
(the  basis  of  all  knowledge)  is 
acquired  early  in  life.  The  na- 
ture of  the  process  is  entirely 
unknown,  but  it  rests  upon  the 
power  of  storing  up  memories 
and  of  recalling  them  at  will.  It 
depends  upon  the  integrity  of  the 
central  and  peripheral  sensory 
neurons  (463-4),  as  well  as  upon 
that  of  the  terminal  sensory  or- 
gans and  of  the  cerebral  cortex 
(47  to  56).  This  power  may  be 
diminished,  or  exaggerated,  or 
perverted  in  various  diseases. 


345  DIMINUTION 

Either  no  perception  or  an  abnor- 
mally feeble  one  follows  a  sensory 
irritation  adequate  in  health  to 
cause  a  perception  (805,  810). 


346  EXAGGERATION 

An  unusually  strong  perception,  as 
compared  with  health,  follows  any. 
sensory  irritation  (806). 


347  PERVERSION 

The  occurrence  or  modification  of  a 
percept  ion  such  as  never  occurs  in 
health  (930). 


The  conditions  under 
which  sensation  may 
be  diminished  or  in- 
creased are  set  forth 
in  Chart  VI  a. 


The    conditions    under 
which    sensation    is 
perverted   are  set 
forth    in 
Chart  VI  b. 


87 


CHART  VI  a 

Diminution  and  Exaggeration  of  Sensation 

Comprising  Numbers  345  and  346,  and  348  to  372 


89 


ANALYSIS  OF  THE  OBJECTIVE  SYMPTOMS  OF  THE  CASE  (SEMEIOLOGY) 


SENSATION 

Diagnostic 

Symptoms  Definition 

348  A  loss,  or  diminution,  of  the 

Anesthesia  normal  sensibility  to  touch 

(complete)  or      upon     adequate     irritation. 

Hypesthesia        Normal  sensibility  varies  in 

(partial).  acuteness  in  different  parts 

(Superficial         of  the  body  and  in  different 

sensibility)  individuals. 


349 

Analgesia  or 
Hypalgesia 


350 

Thermic 

Anesthesia  or 
Hypesthesia 


A  loss,  or  diminution,  of  the 
normal  sensibility  to  pain, 
which  in  health  varies  in 
different  individuals  and  in 
different  parts  of  the  body. 

A  loss,  or  diminution,  of  the 
sensibility  to  variations  in 
temperature.  This  loss  may 
be  more  marked  for  cold 
than  for  heat  and  vice  versa. 


353 

Apallesthesia  or 
loss  of  osseous 
sense  or  vibra- 
tion sense. 

354 

Astereognosis 


355 

Deafness  or 
Anakusia  or 
Hypakusia 

356 

Anosmia  or 
Hyposmia 

357 

Ageusia  or 
Hypogeusia 

358 

Blindness  or 
Anopsia  or 
Amaurosis 

359 

Amblyopia 


Significance 
Diminution  of  sensibility  may  be  clue  to 
disease  of  the  terminal  end  organs,  or  to 
a  destructive  lesion  either  of  the  peri- 
pheral sensory  neurons  (464),  (in  which 
case  all  forms  of  sensibility  are  abolished 
over  an  area  usually  coinciding  with, 
but  smaller  than,  the  distribution  of  a 
peripheral  nerve,  and  the  reflex  acts  in 
the  same  part  are  also  abolished);  or  of 
the  sensory  central  neurons  (463),  (in 
which  case  frequently  all  forms  of  sensi- 
bility are  not  abolished,  and  the  anes- 
thetic area  does  not  correspond  to  the 
area  of  distribution  of  a  nerve,  and  the 
reflex  acts  in  the  part  are  not  abolished). 
Sensibility  is  abolished  in  coma,  nar- 
cosis and  often  apparently  in  hysteria.  A 
broad  zone  of  analgesia  and,  more  rarely, 
of  anesthesia  also,  about  the  body  occurs 
in  locomotor  ataxia:  "tabetic  cuirass." 
The  anesthetic  area  may  coincide  with 
the  distribution  of  a  peripheral  nerve  or 
with  that  of  a  nerve  root  (peripheral 
lesion);  or  with  the  distribution  of  sev- 
eral nerve  roots  (spinal  lesion) ;  or  the  area 
may  involve  one-half  the  body:  called 
hemianesthesia  (cerebral  lesion  and  hys- 
teria). Anesthesia  of  one  side  of  the  face 
and  of  the  opposite  arm  and  leg,  "crossed 
hemianesthesia,"  occurs  in  lesions  in  the 
tegmentum  of  the  pons.  Anesthesia  may 
involve  some  portion  of  the  body  sup- 
plied by  small  branches  of  many  different 
nerves,  such  as  a  hand,  a  foot,  a  leg,  a 
forearm,  etc.,  and  be  sharply  limited 
"stocking  and  glove  variety"  (hysterical). 
(Fig.  33.) 

Analgesia,  thermic  anesthesia  and  apalles- 
thesia may  be  due  to  lesion  of  the  central 
gray  matter,  or  of  the  antero-lateral  as- 
cending tract,  of  the  cord.    (Fig.  26.) 

Loss,  or  diminution,  of  sense     Astereognosis  always  indicates  a  lesion  of 
of  hearing.  the  cerebral  cortex.     (Fig.  15.) 


351  Inability  to  distinguish  differ- 
Loss  of  pressure     ences  in  the  amount  of  pres- 

sense  sure  made  on  the  skin. 

352  Inability  to  tell  how  strongly  a 
Loss  of  muscle        muscle  is  contracted,  wheth- 

and  joint  sense  era  joint  is  flexed  orextended, 
or  Akinesthe-  or  where  an  extremity  is  sit- 
sia.  (Deep  uated  in  space.  A  very  corn- 
sensibility)  plex  sensation. 


Inability  to  feel  the  vibration 
of  a  tuning  fork  pressed  firm- 
ly on  the  skin. 


Inability  to  recognize  objects 
by  the  sense  of  touch;  anes- 
thesia not  being  present. 


Loss,  or  diminution,  of  sense  of 
smell. 


Loss,  or  diminution,  of  sense 
of  taste. 


Loss  of  vision. 


Decided  impairment,  but  not 
complete  loss,  of  vision,  espe- 
cially for  colors  in  the  early 
stages.  Usually  in  such  cases 
the  field  of  vision  is  made 
small  by  the  loss  of  more  or 
less  of  its  periphery  or  by 
scotomata. 


Anakusia,  anosmia,  ageusia  and  blindness, 
may  be  due  to  a  lesion  of  the  sensory 
terminal  organ,  of  the  sensory  nerve  or 
tract,  or  may  be  functional.  But  these 
symptoms  may  occur  in  so  many  condi- 
tions unconnected  with  the  nervous  sys- 
tem that  they  may  have  very  little 
diagnostic  value  in  nervous  diseases. 

Hemeralopia  associated  with  a  central  sco- 
toma for  green  and  red  is  not  uncom- 
mon in  tobacco  smokers;  so  that  when 
the  pupil  is  dilated  in  a  dim  light  the 
health  part  of  the  retina  can  act.  This 
condition  is  quite  different  from  snow- 
blindness,  where  the  retina  is  exhausted 
by  too  bright  and  too  long  continued 
light. 

Nyctalopia  is  at  times  associated  with  con- 
genital retinitis  pigmentosa,  with  cor- 
tical (peripheral)  cataract  and  with  other 
defects  in  the  eye. 


90 


SENSATION  (Continued) 


Diagnostic 
Symptoms 

f  360 

Hemeralopia 


361 

Nyctalopia 

362 

Hemianopia 


Definition 
A  condition  in  which  the  pa- 
tient sees   better  in  a  dim 
light  than  in  a   bright   one 
(day  blindness). 


A  condition  in  which  the  pa- 
tient sees  well  in  a  bright 
light  but  is  almost  blind  in 
a  dim  one  (night  blindness). 


Loss  of  one-half  of  the  field  of 

vision. 
Homonymous  Loss  of  the  same  half  in  both 

fields. 
Nasal  Loss  of  the  nasal  half  in  each 

or  either  field. 
Bi-temporal     Loss  of  the  temporal   half  in 

both  fields. 


363 

Tetartanopia 
or  Quadrantic 
Hemianopia 


Loss  of  an  homonymous  quad- 
rant of  both  fields  of  vision. 


364  Inability    to    distinguish    the 

Achromatopsia       different    colors    from    each 

or  color  blind-    other  either  throughout  the 

ness.      Hemi-     whole,  or   in    one-half     the 

chromatopsia      field  of  vision. 


365 

Dissociation 
of  sensation 


366 
Hyperesthesia 


367 
Hyperalgesia 

368 

Thermic  Hyper- 
-ia  or 
Hyperalgesia 

360 
Hyperosmia 

870 

llyprrgcusia 

371 
Photophobia 

872 
Byperakusia 


Loss  of  some  forms  of  cutane- 
ous sensibility  (usually  for 
pain  and  temperature)  with 
preservation  of  others  (tac- 
tile).    (Figs.  24-7.) 

Increased  tactile  sensitiveness. 
An  unusually  slight  touch 
can  be  perceived.  A  very 
rare  and  even  doubtful  con- 
dition. It  is  usually  employed 
when  a  touch  causes  an  un- 
usually great,  even  painful 
sensation,  where  hyperalge- 
sia or  haphalgesia  (380) 
would  be  a  better  term. 

Increased  sensitiveness  to  pain. 


Increased,  even  painful,  sensi- 
tiveness to  heat  or  cold,  or 
both. 

Increased.  e\en  painful,  sensi- 
tiveness to  odoi 

ed  and  unpli  asant  Ben* 
Bitivenesfl  to  taste. 


Significance 
Homonymous  hemianopia  is  due  to  a  lesion 
of  the  optic  tract  posterior  to  the  chiasm, 
of  the  geniculate  bodies,  the  optic  fascicu- 
lus or  the  median  surface  of  the  occipital 
lobe  of  the  opposite  side  of  the  brain 
(lips  of  calcarine  fissure).     (Fig.  16) 

Bi-temporal  hemianopia  is  due  to  a  lesion 
of  the  central  part  of  the  optic  chiasm. 
Nasal  hemianopia  is  due  to  a  lesion  of 
the  lateral  margin  of  the  optic  chiasm. 
Bi-nasal  hemianopia  cannot  result  from 
one  lesion. 

Tetartanopia  is  due  to  a  lesion  of  the 
upper  lip  of  the  contralateral  calcarine 
fissure  if  it  be  a  lower  quadrant  of  the 
field  of  vision  and  of  the  lower  lip  of 
this  fissure  if  it  be  an  upper  quadrant; 
very  rarely  to  a  partial  lesion  of  the 
geniculate  bodies  or  optic  fasciculus. 
(Fig.  16.) 

Achromatopsia  may  be  due  to  a  congenital 
defect  or  to  defective  education  or  may 
be  the  early  stage  of  a  gradually  devel- 
oping blindness  or  amblyopia.  Due  to 
mild,  not  completely  paralysing,  lesions 
of  any  portion  of  the  visual  tract  in  the 
broad  sense. 

Dissociation  of  sensation  always  indicates 
a  lesion  of  the  central  gray  matter 
(syringomyelia)  or  of  the  lateral  col- 
umns of  the  spinal  cord,  or  more  rarely 
a  lesion  in  the  ponto-cerebellar  angle  of 
the  pons  at  the  level  of  the  auditory 
nerve.  It  occurs  associated  with  motor 
paralysis  of  the  opposite  side  of  the  body 
in  some  cases  of  Brown-Sequard's  paral- 
ysis. 


i  at  ion  of  sensibility  of  all  kinds  is 
usually  functional.  More  rarely  it  is  the 
result    of    an    irritative,    rather    than    a 

destructive,    lesion    of    the   oentral    or 

peripheral  sensory  neurons.  It  occurs 
in    Strychnine     poisoning    and     tetanus. 

Byperesthesia  occurs  as  a  zone  at  the 
upper  limit  of  the  anesthesia  in  many 

spinal    lesions,   and   on   the  same  side   of 

the  body  as  is  the  lesion  In  Brown- 
S&ruard'a  paralysis.  It  is  usually  asso- 
ciated with  increased  reflex  activity. 

Photophobia  is  functional,  or  due  to  eye 
strain,  or  to  inflammation  of  some  part 

of   the   eye,   nr   optic   nerve,   or   cerebral 

menu 


ed     and     painful    sensi-      \  [  vperakiisia    is    functional,    or   due    to   ear 

tiveneas  to  light,  'diseases   affecting  the  labyrinth,  or  to 

cerebral  conditions  causing  hyperemia  of 
ed,  even  painful,  send-        the  labyrinth   (meningitis,  encephalitis, 

tiveneSS  to  sounds.  tumors,  etc)  and  to  spinal  affections. 


Methods  f<.r  the  detection  of  these  conditions  an  di  scribed  to  chart  [o. 
Diseases  in  which  these  conditions  oocui  ed  in  Chart   XIV. 


CHART  VI  b 

Perversions  of  Sensation 

Comprising  Numbers  347  and  374  to  392 


93 


ANALYSIS  OF  THE  OBJECTIVE  SYMPTOMS  OF  THE  CASE  (SEMEIOLOGY) 


Diagnostic 
Symptoms 
374 
Pain 

(Figs.  33, 
38) 


SENSATION 

Definition 
Is  an  unpleasant  sensation  not  felt  in 
perfect  health,  except  in  cases  of 
injury.  It  varies  greatly  in  intensity. 
It  presents  different  qualities,  such 
as:  tearing,  cutting,  burning,  throb- 
bing, darting,  etc.  It  may  be  diffuse, 
or  felt  in  a  small  area  (localized),  or 
may  run  along  a  nerve  trunk  (radiat- 
ing), or  may  run  half  way  or  entirely 
about  the  body  or  an  extremity  (gir- 
dle) ,  or  it  may  be  felt  in  an  area  which 
is  itself  anesthetic  (anesthesia  dolo- 
rosa). Pains  may  vary  as  to  time  of 
occurrence,  some  showing  a  distinct 
periodicity  (malaria,  neuralgia  and 
migraine),  some  occur  at  menstrual 
epochs.  Some  headaches  occur  in 
morning  (uremic) ,  others  in  afternoon 
(ocular)  and  others  towards  evening 
and  at  night  (syphilitic).  Some  pains 
are  increased  by  pressure  (neuritis 
and  neuralgia)  while  some  are  dimin- 
ished by  it  (lead  colic). 


375  Curious  sensations  rarely  felt  in  per- 

Paresthesiae  feet  health,  usually  unpleasant  but 
not  severe  enough  to  be  called  pain. 
They  are  numbness,  tingling,  formi- 
cation, heat,  cold,  heaviness,  tired 
feeling,  hunger,  etc. 

376 

Failure  of  When  a  cutaneous  sensation  is  felt  but 
localization   cannot  be  localized. 

(Topoanesthesia) 


377 

Allocheiria 

378 

Double  sen- 
sation and 
Polyes- 
thesia 

379 

Paradoxical 
sensation 


When  "an  irritation  is  not  felt  at  the 
point  of  contact,  but  at  a  correspond- 
ing point  on  the  opposite  side  of  body. 

Where  one  contact  gives  rise  to  two 
distinct  sensations  (double  sensation) 
or  more  (polyesthesia). 

The  quality  of  thermic  sensation  is 
reversed,  a  hot  body  feels  cold  and 
vice  versa. 


380  A  slight  tactile  impression  from  certain 

Haphalgesia      objects,  but  not  from  others,  is  felt 

as  intense  pain. 
381 
Retardation  The  sensation  of  pain  is  not  felt  until 

of  conduc-     an  appreciable  interval  after  the  time 

tion  of  pain  of  contact. 

382  The  sensation  continues  an  unusually 

Persistence        long  time  after  the  irritation  causing 
of  sensation   it  has  ceased  to  act. 


Significance 
Perversions  of  sensibility,  especially 
pain  and  paresthesiae,  are  often 
functional  and  are  often  due  to 
irritation  (pressure,  chemical,  in- 
flammatory, etc.)  of  central  or  peri- 
pheral sensory  neurons.  Radiating 
and  girdle  pains  are  usually  due  to 
lesions  of  the  nerve  roots.  Anes- 
thesia dolorosa  is  due  to  a  lesion  of 
the  central  end  of  a  sensory  neuron 
which  has  been  destroyed  below  this 
point  and  therefore  can  conduct  no 
sensations  from  below. 

Although  pain  may  be  felt  as  peri- 
pheral it  may  be  of  central  origin  and 
due  to  lesions  of  central  neurons 
within  the  brain  or  cord.  On  the 
other  hand  pains  due  to  lesions  in  the 
abdominal  viscera  may  be  referred  to 
remote  parts  of  the  body  or  the  head 
(referred  pains  952). 

Failure  of  localization  may  be  func- 
tional but  usually  results  from 
lesions  of  the  peripheral  sensory 
neurons  (tabes). 

Allocheiria  occurs  in  hysteria,  very 
rarely  in  tabes,  hemiplegia  and 
sclerosis. 

Polyesthesia  occurs  only  in  tabes  and 
in  hysteria. 

Paradoxical  sensation  has  been  met 
with  in  a  number  of  spinal  and  cere- 
bral diseases,  but  is  without  diag- 
nostic significance. 

Haphalgesia  occurs  in  hysteria. 

Retardation  of  conduction  of  pain 
occurs  only  in  lesions  of  peripheral 
sensory  neurons  (tabes  or  multiple 
neuritis). 

Persistence  of  sensation  occurs  in 
lesions  of  the  peripheral  sensory 
neurons  (tabes). 

Binocular  diplopia  is  due  to  a  weak- 
ness of  one  or  more  of  the  external 
muscles  of  one  eye,  or  to  displace- 
ment of  one  eyeball;  so  that  the 
image  does  not  fall  on  identical  spots 
in  the  two  retinae. 


94 


SENSATION  (Continued) 


Diagnostic 
Symptoms 
383 
Binocular 

Diplopia 

(816) 


384 

Monocular 
Diplopia 
or  Poly- 
opia (878- 
82) 

385 

Metamor- 
phopsia 

386 
Micropsia 

387 
Macropsia 

388 

Tinnitus 
Aurium 

389 
Parakusis 


Definition 
Two  separate  visual  perceptions  of  the 
same  object,  the  perception  from 
the  normal  eye  (true  image)  being 
more  distinct  than  that  from  the 
abnormal  eye  (apparent  image). 


A  condition  in  which  objects  appear 
double  or  multiple,  even  when  looked 
at  with  one  eye  alone. 


A  condition  in  which  objects  appear 
distorted. 


A  condition  in  which  everything  looks 
much  smaller  than  normal. 

A  condition  in  which  everything  looks 
much  larger  than  normal. 

A  sound  of  ringing,  roaring,  whistling, 
etc.,  in  ears  or  head. 


Perversions  of  hearing,  such  as  hearing 
tones  incorrectly  or  hearing  better 
when  other  loud  noises  are  present  at 
the  same  time,  or  hearing  sounds  or 
words  for  which  there  is  no  external 
cause  (hallucination). 

390  The    perceptions   of    abnormal    odors 
Parosmia  or    of   those  for  which  there  is  no 

external  cause  (hallucination). 

391  The    perception    of    abnormal    tastes 
Parageusia        or  of  those  for   which    there  is  no 

external  cause  (hallucination). 

392  A  feeling  as  if  the  person  (subjective) 
Vertigo  or  as  if  BUrrounding  objects  (objec- 
tive) were  whirling  about,  or  both. 


Significance 
Monocular  diplopia  may  occur  in  hys- 
teria, in  cases  of  double  pupillary 
opening,  in  anomalous  refraction 
(incipient  cataract),  and  irregular- 
ities in  the  cornea. 

Metamorphopsia  may  occur  in  hysteria, 
also  in  astigmatism  (refractive)  and 
in  displacement  of  the  retinal  ele- 
ments (retinal)  which  may  occur  in 
retinitis,  choroiditis,  and  in  detach- 
ment, or  tumor,  of  retina. 

Micropsia  may  occur  in  hysteria,  in 
paralysis  of  accommodation  and, 
with  distortion,  when  the  retinal 
elements  are  spread  apart  (recent 
choroiditis  or  retinitis). 

Macropsia  may  occur  in  hysteria,  in 
spasm  of  accommodation  and,  with 
distortion,  when  the  retinal  elements 
are  crowded  together  (atrophic  stage 
of  retinitis  and  choroiditis). 

Tinnitus  aurium,  parakusis,  parosmia 
and  parageusia  occur  in  lesions  of  the 
terminal  organ  and  in  insanity  and 
functional  disorders.  They  may  con- 
stitute the  aura  of  an  epileptic  attack. 

Vertigo  may  be  functional  (hysteria, 
neurasthenia, traumatic  neuroses); or 
may  depend  on  changes  in  the  cere- 
bral circulation,  especially  anemia 
and  hyperemia  (cardiac  ami  arterial 
diseases,  congestion  in  portal  orsys- 
temic  circulation,  galvanism  of  head 
orneck),  or  toxic  (tobacco,  morphine, 
alcohol,  some  digestive  disturbances, 
etc.) ;  or  may  depend  on  diseases  of 
the  cerebellum  and  its  tracts,  or  of  the 

ear  or  eye.  It  is  the  principal  symp- 
tom in  Meniere's  disease  (aural  ver- 
tigo). Vertigo  is  closely  associated 
with  vomiting.  In  vertigo  associated 

with  lesions  in.  or  pressing  upon,  a 

cerebellar  hemisphere,  externa]  ob- 
jects seem  to  whirl  in  (lie  direction 
away  from  the  injured  hemisphere  in 

both  conditions,  hut  the  subjective 
vertigo,  usually,  is  away  from  the 

injured     hemisphere     in     case     the 

lesion  is  within  it  and  towards  it 

when    the    lesion    is    external    and 

presses  upon  t  he  hemisphere. 


hi  <  :i   .      mi   winch   these  condition-  occur  are  discussed  in  Charts   XIV  and    XV 


95 


CHART  VII  a 

Electrical  Examination 

Comprising  Numbers  395  to  405 


97 


ANALYSIS  OF  THE  OBJECTIVE  SYMPTOMS  OF  THE  CASE  (SEMEIOLOGY) 
Definition,  Significance  and  Relationship  of  the  Symptoms  of  Disease 


Name 

Tis- 

Reaction 

OF  THE 

sue 

to 

Reac- 

Test- 

Faradism 

tion 

ed 

395 

'396 

- 

'Contraction  " 

ELECTRICAL 

Normal 

present  to 

REACTION 

excita- 

a strength 

OF  MUSCLES 

bility 

of  current 

AND  NERVES 

(473) 

which  is 

(70-3) 

normal  for 

Nerve  fibers 

thejnerve 

respond  to 

N 
E 

and  muscle 

changes  in 

tested. 

intensity  of 

R 

both  the  far- 

V 

Cont  raction 

adic  and  the 

397 

E 

present  but 

galvanic  cur- 

Dimin- 

A 

it  requires 

rents.    The 

ished 

N 

an  unusually 

changes  in 

excita- 

D ' 

strong 

intensity  are 

bility 

M 

current  to 

best  brought 

U 

produce  it. 

about  by 

s 

making  and 

c 

L 

E 

breaking  the 

current. 

Muscle  fibers 

398 

respond  only 

Exag- 
gerated 

to  the  galvanic 

Contraction 

current.   The 

excita- 

present to  an 

muscle  re- 

bility 

unusually 

sponds  to  the 

weak 

faradic  current 

.current. 

only  in  virtue 

of  the  nerve 

fibers  supplied 

to  it.    When 

these  nerve 

fibers  are  de- 

Gradual 

generated  the 

loss  of 

muscles  can  no 

excitability 

longer  respond 

which  be- 

to the  faradic 

f  N 

comes  com- 

current.    Both 

E 

plete  in 

nerves  and 

R 

about 

muscles  have 

V 
E 

two  weeks 

points  on  the 

after  injury 

body  surface; 

399 

or  onset  of 

the  so-called 

Reac- 

the disease.  . 

motor  points 

tion  of    . 

(see  figures  1  to 

degen- 

Gradual 

5)  from  which 

eration 

loss  of 

they  are  most 

(472) 

M 
U 

s 

excitability 

readily  excit- 

which be- 

able.  There- 

c 

comes  com- 

fore, in  testing 

L 

plete  in 

a  nerve  or 

..  E 

less  than 

muscle  by 

two  weeks 

electricity  the 

after  injury 

electrode  (pos- 

or onset  of 

itive  or  nega- 

the disease. 

tive)  is  placed 

on  the  corre- 

sponding 

motor  point 

(70-3). 

Reaction  to  Galvanism 
and 
Formula  of  Galvanic  Reaction 

Neg.Cl.C.  Pos.Cl.C.  Pos.Op.C.  Neg.Cl.Tet 
is  the  normal  formula,  or  in  other  words 
Neg.Cl.C.  occurs  with  the  weakest  cur- 
rent that  will  cause  any  contraction. 
Neg.Cl.C.  Pos.Cl.C.  with  a  little 
stronger  current.  Neg.Cl.C.  Pos.Cl.C. 
Pos.Op.C.  with  a  still  stronger  current. 

The  explanation  of  the  above  formula 
is  as  follows:  The  weakest  current 
that  will  cause  any  contraction 
of  the  muscle  will  do  so  when  the 
negative  electrode  is  on  the  motor 
point  and  the  current  is  closed.  (Neg.- 
Cl.C.) A  more  powerful  contraction 
will  take  place  when  a  stronger 
current  is  used  and  then  there  will 
also  be  a  contraction  when  the  current 
is  closed  and  the  positive  pole  is  on 
the  motor  point  (Pos.Cl.C).  A  still 
more  powerful  current  causes  a  con- 
traction when  the  current  is  opened 
and  the  positive  electrode  is  on  the 
motor  point  (Pos.Op.C).  With  such 
powerful  currents  and  the  negative 
pole  on  the  motor  point  there  results 
a  tetanus  or  continuous  contraction 
when  the  current  is  closed,  (Neg.Cl. 
Tet.) ;  so  that  the  muscle  cannot  relax 
to  contract  again  when  the  current 
is  opened-  There  is,  therefore,  in 
health  no  reaction  corresponding  to 
"  Neg.Op.C" 


No  reaction. 

After  the  first  two  weeks  the  muscle 
responds  to  unusually  feeble  gal- 
vanic currents  and  the  normal  form- 
ula is  reversed;  the  positive  pole  be- 
ing more  potent.  Pos.Cl.C.  Neg.Cl. 
C.  Pos.Op.C  Neg-Op.C  (which  last 
reaction   never   occurs   in   health). 

It  is  usual  to  express  the  formula 
for  the  normal  reaction  and  for  the 
reaction  of  degeneration  in  the  Ger- 
man language  in  which  Kathode 
means  the  negative  electrode  and 
Anode  means  the  positive  electrode. 
The  usual  normal  formula  is 
K.C.C,  A.C.C,  A.O.C,  K.C.Te. 
The  reaction  of  degeneration  is 
A.C.C,  K.C.C,  A.O.C,  K.O.C 
The  essence  of  the  normal  formula 
is  K.CC>A.CC  The  essence  of 
the  formula  of  the  reaction  of  degen- 

.    eration  is  A.CC>K.CC 

98 


Character  Significance 
of  the  of  the 

Contrac-       Reaction 
tion 

"Normal 
excitability 
shows  a 
normal 
condition 
of  muscle 
and  nerve. 


Diminished 
excitability 
occurs  in 
many  dis- 
eases and 
conditions, 
especially  in 
lesions  of 
the  central 
motor  neu- 
rons and  is 
not  of  much 
value  in 
diagnosis. 


Quick. 


None. 

Sluggish. 
The 


character 
of  the 
muscular 
contrac- 
tion is 
the  most 
charac- 
teristic 
thing  in 
the  reac- 
tion of 
degen- 
eration. 


Exaggert  ted 
excitability 
is  a  rare 
condition.    It 
occurs  in 
nervous 
persons  with 
moist  skins 
and  in  tetany. 

The  reaction 
of  degenera- 
tion proves 
that  the  peri- 
pheral motor 
neurons  are 
degenerated 
and  that  re- 
covery will 
either  never 
take  place, 
or  will  be 
very  slow. 
The  lesion 
must  be 
either  in  the 
peripheral 
nerves,  or 
nerve  roots, 
or  in  the 
anterior 
horns  of  the 
spinal  cord, 
or  in  the 
motor  nuclei 
in  the  brain 
stem. 


ELECTRICAL  REACTIONS  (Continued) 


Character 

Name 

Reaction 

Reaction 

Formula  of 

OF  THE 

.Significance 

OF  THE 

Tissue 

to 

to 

Galvanic 

Contrac- 

of the 

Reaction 

Tested 

Faradism 

Galvanism 

Reaction 

tion 

Reaction 

■ 

Contractions 

present,    but " 

Either  the 

Quick  or 

The  signifi- 

Nerve 

require  unusually  strong 

normal    form- 

sluggish 

cance  of  this 

currents,  w 

tiether  faradic 

ula,  or  the 

reaction  is 

400 
Partial 

or  galvanic- 

formula  of  the 

the  same  as 

reaction  of 

that  of  the 

reaction    " 
of  degen- 
eration 

Contractions 

Contractions 

_  degeneration, 

reaction  of 

present  only 

present  to 

or  a  combina- 

degeneration, 

Muscle 

to  unusually 

unusually 

tion  of  the  two 

Sluggish. 

except  that  it 

strong  cur- 

weak cur- 

mav be  pres- 

indicates the 

rents. 

rents 

ent*.      A.C.C. 
may  equal 
K.C.C. 

lesion  is  less 
severe  and 
that  all  the 
nerve  fibers 
are  not  de- 
generated. 

401 

Myas- 

Nerve 

Contractions 

Normal 

Normal. 

Quick, 

Occurs  only 

thenic 

and 

quickly  grow 

grows 

in  myas- 

reaction 

Muscle 

less  strong 

rapidly 

thenia  gravis 

(553) 

and  soon 
cease  under 
rapidly 
repeated 
excitation. 

weaker 

and 

ceases. 

(553). 

402 

Myo- 

Nerve 

Continuous 

Curious 

Positive  pole 

Continues 

Occurs  in 

tonic 

and 

tonic  con- 

wave-like 

is  about 

usually  a 

Thomsen's 

reaction 

Muscle 

traction 

contractions 

equally  as 

long  time 

disease 

(613) 

lasting 

occur,  and 

potent  as  the 

and  has  a 

(613). 

Bome  time 

last  after 

negative. 

wave-like 

after  the 

electrical 

Hence  the 

character. 

electrical 

stimulation 

formula 

stimulation 

has  ceased. 

A.C.C.  =  K.C.C. 

has  ceased. 

403 
Neuro- 
tonic 

reaction 


'Nerve      Unusually  excitable.      Te- 


tion  has  ceased. 


404 

Heart  ion 

pletely 

lerated 

muscle 

(70  to  73) 


Muscle     Normal. 
Muscle     None. 


tame  contraction  persists  I 
after   electrical    stimula- 

V  Normal. 

I 


Normal. 
None. 


Nunc 


Continuous 


None. 


Occurs  in 
hysteria, 
amyotrophic 
lateral 

sclerosis  and 
chronic  bul- 
bar paralysis. 

Muscle  fibers 
are  entirely 
degenerated 
and  recovery 
is  impossible. 


W5 

Electrical 
reaotion 
of  the 
i  ipticand 

Auditory 

Nerves 


•The  optio  nerve  reapondi  to  the  garranio  current  with  :i  teniatlon  of  light,   the  ootor  <>f  whiob 
ranee  with  the  pole  empli 

The  auditory  nerve  reaponda  with  ■  loud  Kundwbeo  the  Motive  electa 
tho  meat  hi  and  the  current  do  ed  end  with  ;i  feint  sound  wood  the  poeltive  pole  la  need   end    i 
itrooger  current  broken.    Theee  reaction*  are  withou  Importance. 

The  negative  electrode  placed  in  front  of  thai  I  when 

the  current  M'i.>.-.|  mlintl ppoeite  direction  when  the  ourrenl   e.  broken     The  p 

•    electrode  <  Ij  the  revet  ■  direction, 

in  which  the  caloric  U  and  is  "Inch  the  electric  teal 

tii  1  \  certain  thai  the  lesion  is  in  the  labyrinth  and  not  m  the  oerve 

If  there  is  qo  ri   pon  e  to  either  the  calorie  or  the  electric  test  the  lesion  is  in  the 

oerve  or  its  nuoleus. 

99 


CHART  VII  b 

Erb's  Motor  Points  for  Electrical  Examination  of 
Nerves  and  Muscles 

The  motor  points  arc  the  areas  upon  the  surface  of  the  body  at  which  the  individual  nerves  and 
muscles  can  be  most  easily  excited  by  electricity.  For  the  nerves,  these  points  coincide 
with  those  al  which  the  nerve  lies  most  superficially  or  where  it  can  be  pressed  against  a 
resisting  tissue;  for  the  muscles,  they  lie  over  the  point  of  entrance  of  the  nerve  into  the 
muscle. 

Comprising  Figures  1  to  5 


101 


ERB'S  MOTOR  POINTS 


M.  orbic.  palpebr. 

Muscles  or  the  ( 

nose  \ 

M.  zygoruatici 
M.  orbicul.  oris< 
Middle  branch  of 
facial 

M.  niasseter 

M.  levator  rocnti 

M.  quadr.  menti 

M.  triang.  menti 

JV.  hyyixilosx. 

JjOtcer  branch  of 

facial 

M.  platysma 

mvoides 

Muscles  of  the  f 

root  of  tongue  \ 


M.  omobyoideus 


JV.  thoracic,  anter. 
(M.  pector.) 


N.  phrenicus 


Suprascapular 
poiDt.     (Erb's  point. 
M.   deltoid.,    biceps, 
brachial,  intern,  and 
supinat.  long.) 

Rg.i 


third  frontal 
convolution, 
M.  temporalis 
Upper  branch  of 
facial  in  front 
of  car 
X.  facialis 

N.  auriculo.  post. 
Middle  branch  of 

facial 
Loner  br.  of  facial 
M.  splenitis 
M.  sternoeleido- 

mastoideus 
N.  accessorius 

M.  levator  anguli 
scapulae 

M,  cucullaris 

JV.  dors,  scapula? 


N.  thoracic,  long. 
(M.  serratns 
antic,  maj.) 


M.  >leltoideua 


M    )Dist>ric»te* 


ERB'S  MOTOR  POINTS     (Continued) 


Fig.  3 


U   kdtludor  magnua 
M.  .idduct.  longu;, 


M    'vim  l»ternui 


M.  tensor  facie  lit* 


Fig.  4 


M   blcrp*  tm    <r»|v  brvv 


M    B>tor  bAllitfn  h,(.r. 


CHART  VII  c 


ERB'S  DIAGRAM  SHOWING  THE  EFFECTS  OF  INJURY  OF  A  NERVE 


V,lu»^- 


> — *■ —      ," — ^     ,      ,.     V     i      »     » — v — ,.,      — ^  i 


ealtk. 

i?      11       A  WyK 


Health       ^WZZr  y3trot)h1)^^-o|1(tr6tioi,offniwle,C»rrkosis      &±£ 


§lGa.lv4nic 
M.u)    . 

£:|f&r<xdic 


y       o       jo      it      jo      *c      io 


Fig.  6 
Charts  Illustrating  the  Reaction  of  Degeneration 

The  star  (*)  indicates  the  incidence  of  a  paralysing  lesion  in  the  domain  of  the  peripheral 
neuron.  Voluntary  motion  is  lost  at  once.  During  the  Oral  two  weeks  there  is  Blight  diminu- 
tion of  the  galvanic  excitability  of  muscle;  there  is  also  rapid  diminution  of  the  faradic  excitability 
of  muscle  and  iif  the  galvanic  and  faradic  excitability  of  aerve,  which  are  completely  lost  at  the 
cud  of'tlie  second  or  third  week.  During  the  second  week  then-  is  rapid  increase  iii  galvanic  ex- 
citability of  muscle  and  the  response  to  the  positive  pole  becomes  greater  than  to  the  negative. 

Chart  1  represents  the  reaction  in  a  ease  terminating  in  recovery.     During  the  sixth  week 

sited  by  the  cross  X)  regeneration  begins.   The  increased  galvanic  excitability  of  the  muscles 

gradually  diminishes  until  it  becomes  normal  and  the  poles  are  reversed  so  thai  the  negative 

nspouse  is  again  greater  than  the  positive.     Voluntary  motion  returns  first,  then  the  galvanic 

and  faradic  excitability  of  the  nerve,  and  laal  of  all,  the  faradic  excitability  of  the  muscl 

Chart  2  represents  the  reaction  in  a  case  terminating  in  atrophy  and  cirrhosis  of  the  muscle. 
The  galvanic  excitability  of  the  muscle  isinoreased  and  the  poles  are  reversed,  as  before.  The  decline 
in  galvanic  excitability  continues,  however,  until  the  end  of  the  second  year,  when  it  is  entirely 
Voluntary  motion,  and  the  electrical  reactions  of  both  muscles  and  nerve  are  thus  perma- 
nently destroyed. 


in;. 


CHART  VIII 

Analysis  of  the  Cerebro-Spinal  Fluid 

Comprising  Numbers  410  to  420 


107 


ANALYSIS  OF  THE  OBJECTIVE  SYMPTOMS  OF  THE  CASE  (SEMEIOLOGY) 
ABNORMAL  CEREBRO-SPINAL  FLUID 


Character- 
istics 


410 
A 
B 
N 
O 
R 
M 
A 
L 

C 
E 
R 
E 
B 
R 

O  «! 
i 

s 
p 
I 

N 
A 
L 


411 

Tension 


Mkthod  of  Testing 
Can  be  roughly  estimated  by 
the  rapidity  of  flow  of  fluid 
through  the  canula,  whether 
in  drops  or  a  stream,  more 
accurately  by  the  height  to 
which  the  fluid  rises  in  a  ver- 
tically held  glass  tube  con- 
nected by  a  short  rubber  tube 
with  the  canula.  A  stopcock 
on  the  canula  adds  to  the  ac- 
curacy by  preventing  the 
escape  of  much  fluid  and  the 
consequent  lowering  of  the 
tension.  The  fluid  in  the  tube 
rises  and  falls  with  the  respira- 
tion. An  additional  more 
rapid  and  stronger  pulsation 
indicates  a  basilar  aneurism. 


412 

Red  color 

or 
413 

reddish 

yellow 

color 

414 
Cloudy 


Significance 
A  low  or  very  rapidly  diminishing  tension  has 
no  diagnostic  meaning,  except  as  indicat- 
ing an  obstruction  to  the  communication 
of  the  fluid  in  the  ventricles  with  that  of 
the  vertebral  canal,  as  in  closure  of  the 
foramen  of  Magendie. 

A  high  tension  means  increased  intra-cranial, 
or  intra-spinal,  pressure  caused  by  an  in- 
creased amount  of  cerebro-spinal  fluid  or 
by  a  foreign  body  within  the  cerebro-spinal 
cavity.  It  occurs  in  tumors,  abscess, 
hydrocephalus,  hemorrhage,  acute,  sub- 
acute, some  cases  of  chronic,  and  serous 
meningitis,  also  in  cerebral  edema  (nephri- 
tis, anemia,  etc.),  acute  infectious  diseases 
and  some  other  conditions. 


By  sight.  Fresh  blood  in  the  fluid  may  be  the  result  of  puncture  of  a 

Hematoidin  crys-        blood  vessel,  in  which  case  it  is  most  abundant  in  the 
tals     may     be        fluid  first  drawn,  usually  coagulates,  and  settles  quickly 
seen  under  the        on  centrifugalization. 
microscope.  Or, 

May  be  the  result  of  hemorrhage  into  the  ventricles  or 
membranes.     Hemorrhage,  haematoma,  aneurism,  etc. 


By  sight. 

Pus  cells  under  the  microscope. 

Polymorpho-nuclear  leucocytes. 


415 

Clear  with 
delicate 
coagulum 

416 
Cellular 

elements 

and 

bacteria 


By  sight. 


An  increase  of  cellular  elements  in  the  fluid  is 
usually  the  result  of  an  acute  or  sub-acute 
meningitis.  In  some  cases  of  acute  menin- 
gitis, however,  the  fluid  may  be  clear. 

Tuberculous  meningitis,  usually. 


Fluid  soon  after  withdrawal 
should  be  centrifugalized. 
Tube  should  be  emptied 
quickly  and  from  its  walls  and 
bottom  sediment  should  be 
sucked  in  and  out  of  a  capil- 
lary tube,  well  mixed  and 
spread  on  two  clean  slides. 
One  slide  should  be  stained  by 
Gram's  method  for  bacteria, 
and  the  other  by  Wright's 
blood  stain  for  cellular  ele- 
ments. 

Or. 

The  fluid  (not  centrifugalized) . 
10  parts,  can  be  mixed  with 
1  part  of  a  solution  consisting 
of  methylene  blue  0.2%. 
glacial  acetic  4.0%,  and  watpr 
to  100  %,  and  counted  in  a 
Thoma-Zeiss  chamber. 

108 


The  normal  cerebro-spinal  fluid  shows  under 
these  conditions  1  to  3  cells  in  a  field  of  the 
microscope.  If  there  are  more  than  4  to  6 
cells  in  a  field  it  indicates  a  meningitis. 

If  the  cells  are  mainly  leucocytes  it  indicates 
epidemic  cerebro-spinal,  or  purulent  men- 
ingitis, or  rarely  an  acute  tuberculous 
meningitis.  Broadly  speaking,  an  acute 
infectious  meningitis. 

If  the  cells  are  mainly  or  entirely  lymphocytes 
it  indicates  a  tuberculous  meningitis,  or 
cerebro-spinal  syphilis,  or  paresis,  or  tabes, 
or  acute  anterior  poliomyelitis,  or  conval- 
escence from  any  form  of  acute  meningitis. 
Broadly  speaking  a  chronic  infectious 
meningitis. 

If  echinococcus  cysts  or  hooklets  are  present, 
they  indicate  the  presence  of  an  echinococ- 
cus cyst. 


Character- 
istics 
417 
Sugar 


418 
Albumen 


419 
Globulin 


ABNORMAL  CEREBROSPINAL  FLUID     (Continued) 


Method  of  Testing 
By  Haines'  test  or  other  tests. 


Two  c.c.of  the  fluid  mixed  with 
10  c.c.  of  Esbach's  fluid  is 
centrifugalized  during  one 
hour  in  a  conical  tube  grad- 
uated to  0.1%. 


Significance 
Not  of  much  significance,  but  the  sugar  nor- 
mally   present    is    diminished    usually    in 
meningitis  and  in  some  other  conditions. 

Normally  not  more  than  \%  is  present.  Usu- 
ally increased  in  meningitis  and  tumors. 
A  diminution  in  the  amount  usually  indi- 
cates a  progressive  space-occupying  disease. 
Of  little  diagnostic  significance. 


Two  c.c.  of  a  saturated    solution  of   chemically  pure  neutral  Indicates 
ammonium  sulphate  should  be  placed  in  a  test  tube  and  one  meningitis, 
cc.  of  the  cerebro-spinal  fluid  should  be  gently  run  upon  its  acute  ante- 
top.    If  the  reaction  is  positive,  within  3  minutes,  a  grayish  rior  polio- 
white  ring  should  form  at  the  junction  of  the  two  fluids.    At  myelitis, 
the  end  of  one-half  hour,  the  surface  of  the  ring  should  show  cerebro- 
a  delicate  network.   Best  seen  by  indirect  illumination.  spinal 

Or,  syphilis, 

Boil  slightly  1  volume  of  the  cerebro-spinal  fluid  with  5  volumes  paresis,  tabes, 

of  a  10%  butyric  acid  solution,  add  1  volume  of  a  normal  solu-  rarely  a  brain 

tion  of  sodium  hydroxide,  reheat  and  allow  to  cool.    If  a  floccu-  tumor. 
lent  precipitate  forms,  the  reaction  is  positive.  (Noguchi  test ). 

The  reaction  is  positive  in  U0%  of  cases  of  paresis  and  in  60% 
of  cases  in  talus. 

In  cerebro-spinal  syphilis  both  the  cerebro-spinal  fluid  and  the 
blood  usually  give  a  positive  reaction.  In  other  cases  of  syph- 
ilis (without  meningitis)  the  reaction  is  usually  negative  with 
the  cerebro-spinal  fluid,  but  positive  with  the  blood. 


420 

This  test  can 

Positive 

only  be  per- 

Wasser- 

formed  in  a 

mann 

laboratory 

reaction 

by  an 

expert. 

109 


CHART  IX 

Special  Syndromes  and  Anatomical  Terms 

Comprising  Numbers  425  to  465 


111 


SYNDROMES  AND  SPECIAL  SYMPTOMS  OF  DISEASE 

Syndrome  Definition 

425  Occur  usually  in  self-conscious  females  of  an  emotional  nature.   Lack  of  inhibi- 

Hysterical  tion  and  great  susceptibility  to  suggestion.  Desire  to  excite  admiration  and 
symp-  sympathy  and  wonder.  Mental  instability.  Globus  hystericus  (426).  Spinal, 
toms  inguinal  (or  ovarian)  and  other  tenderness.     Great  variety  of  symptoms 

(1074)  (especially  subjective)  which  cannot  be  explained  by  any  organic  lesion. 
Glove  and  stocking  form  of  anesthesia  or  hemianesthesia  and  concentric 
contraction  of  the  field  of  vision  are  common  symptoms,  but  the  patient 
is  usually  ignorant  of  their  existence  until  they  are  discovered,  or  more 
probably  suggested,  by  the  physician.  Exaggerated  reflexes  but  no  ankle- 
clonus  or  only  pseudo-clonus.  Never  a  Babinski  reflex.  Motor  paralyses, 
tremors,  contractions  and  convulsions  are  not  uncommon.  Transference 
of  hemianesthesia  can  be  effected  in  some  cases.  The  anesthesia  of  the 
fingers  does  not  prevent  delicate  acts  being  done  by  them  with  eyes  closed. 
Such  patients  when  tested  and  the  anesthetic  area  is  touched  often  answer 
"no"  at  the  moment  of  contact  (48).  Many  other  symptoms  do  not  seem 
to  be  real  but  rather  seem  to  be  imaginary  and  may  result  from  hallucina- 
tions or  delusions  or  more  probably  are  the  result  of  suggestion:  auto-,  or 
foreign.  Probably  many  of  the  hysterical  symptoms  come  into  existence 
as  the  result  of  the  physician's  careful  and  minute  examination  or  repeated 
examinations  (foreign  suggestion). 


Signifi- 
cance 


426 

Globus 
Hystericus 
(1074) 

427 

Hystero- 
genic 


The  feeling  of  a  lump  or  ball  behind  the  upper  end  of  the  sternum  which 
interferes  both  with  swallowing  and  breathing.  The  sensation  often  com- 
mences in  the  epigastrium  and  rises  to  the  base  of  the  neck  and  remains 
there;  the  patient  not  being  able  to  get  it  up  or  down.  It  may  be  caused 
by  a  spasmodic  contraction  of  the  muscles  of  oesophagus  or  throat. 

Spots  scattered  over  the  body,  but  usually  in  the  left  inguinal  region,  where 
light  pressure  or  irritation  will  cause  more  or  less  violent  hysterical  attacks 


Hys- 
teria 
(1074) 


areas  (1074) 

42S  Spots  scattered  over  the  body,  but  usually  in  the  left  inguinal  region,  where 

Hystero-        firm  and  continued  pressure  will  cause  the  arrest  of  an  existing  hysterical 

frenic         attack. 

areas  (1074) 

429  A  condition  in  which  the  patient  cannot  move  an  anesthetic  extremity  when 
Lasegue's      her  eyes  are  closed,  but  can  move  it  readily  when  she  opens  her  eyes  and 

symp-        looks  at  it. 
torn  (1074) 

430  The  aura  is  a  symptom  (warning)  which  occurs  before  the  attack  in  about     Epi- 
The  epi-         half  the  cases  of  epilepsy.     It  may  be  remote  or  immediate.    The  former  lepsy 

leptic  is  often  called  "a  prodromal  symptom"  and  occurs  hours  and  days  before  (575,846, 

aura  the  attack.     It  consists  usually  in  an  emotional  change  (irascibility,  etc.),       1058) 

(575,  846,  changes  in  the  amount  of  sleep,  of  food  taken,  in  sexual  desire  and  vaso- 
1058)  motor  phenomena.     Much  more  characteristic  and  important  is  the  imme- 

diate aura  which  occurs  a  fraction  of  a  minute  before  the  attack.  This 
aura  may  be  "psychic"  (anxiety,  anger,  joy.  dreamy  states,  special  thought 
or  memory,  etc.),  or  a  "sensory  hallucination"  which  may  be  visual  (blind- 
ness, lights,  colors  (red),  elaborate  false  visual  perceptions,  etc.),  or  audi- 
tory (deafness,  noises,  and  false  auditory  perceptions),  or  olfactory  or 
gustatory  hallucinations,  or  cutaneous  paresthesiae  (the  feeling  of  a  wind 
blowing  on  some  part  of  the  body  is  quite  common)  and  pains,  or  visceral 
paresthesiae,  especially  epigastric.  Vertigo  is  a  common  immediate  aura; 
or  the  immediate  aura  may  be  motor  and  consist  in  twitching  of  a  group 
of  muscles,  (Jacksonian  epilepsy),  or  in  more  complicated  automatic  move- 
ments of  the  body,  or  in  hiccough,  sneezing,  yawning  or  swallowing.  Vaso- 
motor disturbances,  flushing  or  pallor  with  secondary  paresthesiae,  are  not 
uncommon  immediate  aurae.  Usually  the  aura  is  always  the  same  in  the 
same  individual;  rarely  it  varies.  In  rare  cases  the  aura  may  not  be 
followed  by  an  attack  and  in  still  rarer  and  always  doubtful  cases  it 
may  be  "the  only  svmptom  of  epilepsy. 

112 


SYNDROMES  AND  SPECIAL  SYMPTOMS  OF  DISEASE     (Continued) 


Signifi- 
cance 
Local 
cortical 
lesion 
(587-8, 
605) 


Syndrome  Definition 

431  A  clonic  spasm  of  one  or  more  muscles  in  one  side  of  the  face  or  in  one  arm  or 

Jacksonian    leg,  which  may  remain  local,  but  usually  rather  rapidly  extends  to  other 

epilepsy     muscles  of  the  same  side  of  face,  or  of  the  arm  or  leg  in  which  it  commenced. 

(587-8,       It  then  may  extend  to  an  adjacent  extremity  in  the  same  order  in  which 

605)  the  cortical  centers  are  placed:    thus  from  the  face  to  the  arm  and  then  to 

the  leg,  from  the  leg  to  the  arm  and  then  to  the  face,  from  the  arm  to  the  (Figs.  15- 
leg  and  face  nearly  or  quite  simultaneously,  but  never  from  the  face  to  the  16) 
leg,  or  vice  versa,  without  involving  the  arm.  When  the  spasm  has  ex- 
tended over  the  whole  half  of  the  body  it  may  remain  so  or  may  pass 
across  and  involve  the  other  side.  As  long  as  the  spasm  is  local  or  limited 
to  one-half  of  the  body  consciousness  may  or  may  not  be  lost,  but  when  the 
spasm  involves  both  sides  of  the  body  consciousness  is  always  lost. 


433 

Tabetic 
or  vis- 
ceral 
crises 
(661) 


432  In  many  cases  of  apoplexy,  especially  in  cases  of  cerebral  thrombosis,  the 

The  pro-        apoplectic  attack  is  preceded  by  a  number  of  more  or  less  definite  and 

dromata     characteristic  symptoms  which  may  be  remote,  preceding  the  attack  by 

of  apo-       months  or  years;  or  immediate,  occurring  immediately  before  the  attack. 

plexy  These  prodromata  are  both  general,  such  as  headache,  vertigo,  drowsiness 

(504,  and  stupor,  irritability,  forgetfulness,  hypochondriacal  feelings,  ringing  in 

1060-3)       the  ears,  flashes  before  the  eyes,  etc.;  and  local,  such  as  temporary  attacks 

of  aphasia,  diplopia,   achromatopsia,  dysarthria,  temporary  paralysis  of 

arm  or  paresthesiae.      None  of  these  symptoms  is  so  characteristic  that 

an   attack   of  apoplexy   can   be  confidently  predicted   from   its   presence. 

The  most  constant  prodromal  symptom  of  apoplexy  (except  of  embolism)  is 

high  arterial  tension. 

Paroxysmal  attacks  of  pain  in,  and  functional  disturbances  of, some  viscera,  oc- 
curring in  the  course  of  locomotor  ataxia.  These  attacks  recur  after  irregular 
intervals,  persist  during  an  hour,  or  a  day  or  two,  and  are  analogous  to  the 
paroxysmally  occurring  lightning-like  pains  in  the  legs.  "Gastric  crises" 
are  the  most  frequent  and  consist  in  severe  pain  in  the  epigastrium  together 
with  uncontrollable  vomiting  and  retching.  At  times  attacks  of  gastric 
pain  or  of  vomiting  occur  separately.  "Hepatic  crises"  resemble  gallstone 
colics,  even  being  accompanied  by  slight  jaundice  at  times.  "Laryngeal 
crises"  consist  in  attacks  of  coughing  and  dyspnoea.  "Laryngeal  vertigo" 
(Ictus  laryngeus)  consists  in  a  sensation  of  tickling  and  burning  in  the  larynx, 
a  stridulous  inspiration  with  a  feeling  of  suffocation  and  a  falling  to  the 
ground  unconscious  for  a  few  minutes.  "Pharyngeal  crises"  consist  in  re- 
peated acts  of  noisy  swallowing.  "Banal  i  mble  attacks  of  renal 
colic.  "Vesical  crisis"  consist  in  pain  in  region  of  bladder  and  prostate,  and 
constant  desire  to  urinate.    "Urethral  crises"  consisl  in  attacks  of  pain  in 

Urethra  and  desire  to  urinate.     "Rectal  crises"  consist   iii  attacks  of  pain  in 

the  rectum  and  tenesmus.      "Vulvo-vagmal  crises"  consisl  of  attacks  of 

pain  in  vagina.     "Clitoridian  Orise   "  OOnSlSl  of  attacks  of  pain  in  vulva  with 

ual  desire  and  discharge  of  mucus.    "Anginal  crises"  resemble  angina  pec- 
toris.     Occasionally  if  several   kitnls  occur  simultaneously. 

484  A  combinatii f  several  or  all  of  the  following  symptoms,  dysarthria  or 

Bulbar  anarthria  (283-4),  d  285),  drooling  of  saliva  from  mouth,  propul- 

symp-       si\e  speeeh.  and  puffing,  of  lips.     Paralysis  of  the  7th.  9th,  10th,  I lth,  and 

loin-  12th,  and  at  times  uf  other  cranial  nerves.     Spastic  paraplegia  or  hemiplegia 

(646)         of  extremitii  paralysis  and  ataxia.     Respiratory  difficulty,  and 

m  severe  oases  rapid,  irregular  pulse  and  Cheyne-Stokes'  respiration. 

Long  pauses  iii  the  respiration.     After  a  pau-e  the  respiration  commences  slow 

Cheyne-        and  deep  ami  rapidly  becomes  quick  and  superficial  ami  as  rapidly  becomes 

-low  and  deep  again  and  terminates  in  another  long  pause  (lasting  from  five 
Onds,  or  more)  and  so  on;  each  cycle  being  completed   in  a   few 

tion  mn  pmewhat  similar  respiratory  disturbance  which  is  called  Hint's 

respiration  ooi  equenl  pauses  m  the  respiratory  act.  tasting  many 

oonds.     Hi'"  tion   occurs    m    Bright^   cusease,  etc.,  bul  has  no 

particular  significance  in  aervoiu  diagi 

118 


Apo- 
plexy 
(504, 

1060-3) 


Tabes 

(661) 

(Fig.) 

27 


Lesion 

or  dis- 
order 

med- 
ulla 

Figs 

■J  l   2) 


SYNDROMES  AND  SPECIAL  SYMPTOMS  OF  DISEASE     (Continued; 


Syndrome 
436 

Stokes-Adams'  phenom- 
enon 


Definition 
Slow  pulse  with  long  arrests  (one  half  to  one  minute 
or  more)  during  which  the  patient  becomes  pale, 
unconscious  and  may  show  a  more  or  less  pro- 
nounced convulsion. 


bulbar  syndrome  (1268) 


438 

Ponto-cerebellar  angle 
lesions  (1363) 


437  Paralysis  of  the  tongue,  diaphragm  and  larynx 

Babinski  and  Nageotte's  with  ataxia  of  the  homolateral  side;  analgesia 
and  thermic  anesthesia  with  motor  paralysis  of 
arm  and  leg  of  the  contralateral  side,  myosis 
and  pseudoptosis,  dysphagia  and  dysarthria. 

Homolateral  deafness  and  contralateral  analgesia 
and  thermic  anesthesia  with  preservation  of 
tactile  sensibility,  nystagmus  and  weakness  of 
conjugate  deviation  of  the  eyes  towards  the  side 
of  the  lesion,  anesthesia  and  abolition  of  reflexes 
in  th  ■  distribution  of  the  trigeminus  on  side  of 
lesion,  adiadocokinesia  on  the  same  side,  optic 
neuritis,  cerebellar  ataxia  and  occipital  pains,  all 
more  marked  on  side  of  lesion 

Homolateral  facial  paralysis  with    contralateral 
paralysis  of  arm  and  leg. 

Homolateral  oculo-motor  paralysis  with  contralat- 
eral hemiplegia. 


439 

Millard-Gubler's 
syndrome  (1269) 

440 

Weber's  syndrome  (1270) 


Homolateral  oculo-motor  paralysis  associated  with 
a  tremor  of  the  contralateral  arm  and  leg. 


Significance 
Lesion  of  bundle  of 
His  in  the  heart, 
or  irritation  of 
pneumogastric 
nerve. 

Lesion  of  medulla. 
(Figs.  21-3) 


Lesion  of  ponto- 
cerebellar angle. 
(Fig.  20) 


Lesions   of   pons. 
(Fig.  20) 

Lesion  of  crus 
cerebri. 

Lesion  of  red  nucleus 
or  of  rubro-spinal 


441 

Benedykt's  syndrome 

(1270,  1325)  tract. 

442  Below  the  point  of  lesion  there  are  motor  paralysis,  exaggerated  ten-     Uni- 

Brown-Sequard's      don  reflexes,  Babinski  reflex,  elevation  of  temperature,  vaso-motor     lateral 

paralysis  or  disturbances,  and  at  times  more  or  less  hyperalgesia,  ataxia,  and  loss    spinal 

spinal  of  deep  sensibility  on  the  homolateral  side,  together  with  analgesia,     lesion. 

hemiplegia  thermic  anesthesia,  apallesthesia  (353)  and  more  or  less  tactile  anes-     (Figs. 

(509,  840)  thesia,  on  the  contralateral  side.     The  anesthesia  is  bounded  above     24-6) 

by  a  narrow  zone  of  hyperesthesia  or  hyperalgesia.    Brown-S^quard's 
paralysis  is  more  often  atypical  than  typical. 


443 

Spinal  epilepsy 
(60-1  and  520) 

444 

Bell's  phenomenon 

445 

Strumpell's 
tibialis 


Violent  and  continued  tremor  of  the  leg  after  it 
has  been  struck  or  shaken. 


Greatly  exaggerated 
tendon  reflexes. 


phenomenon 


A  turning  upward  of  the  eyeballs  when  an  attempt     Facial  paralysis 
is  made  to  close  the  eyelids  in  peripheral  facial         (peripheral), 
paralysis. 
When  a  patient,  with  spastic  paralysis  of  a  leg,  lying  on  his  back, attempts" 
to  flex  the  paralysed  leg  at  the  knee  against  light  resistance,  a  dorsal 


446 


flexion  of  the  foot  also  occurs.     Strumpell  has  found  similar  phenom- 
ena in  the  radial  and  pronator  groups  of  muscles  in  the  forearm. 


Babinski 'sasso- When  a  patient  with  spastic  paralysis  of  one  leg,  lying  on  a  hard  surface 
ciated  move-  without  a  pillow,  with  legs  slightly  abducted  and  hands  folded  across 
ments  of  chest,  attempts  to  raise  the  body  to  a  sitting  posture,  the  paralysed  leg 

trunk  and  is  involuntarily  raised  from  its  support  while  the   normal   leg  lies  at 

thigh  rest. 


Lesion 
of  the 
pyra- 

*  midal 
tract. 
Figs. 
24-6) 


114 


SYNDROMES  AND  SPECIAL  SYMPTOMS  OF  DISEASE     (Continued) 


Syndrome 
447 
Argyll-Robertson' 

pupillary  reflex 

(891) 

448 

Romberg's  symp- 
tom (static 
ataxia) 

449 

Biernacki's  sign 

450 

Trousseau's  sign 

451 

Chovstek's  sign 

452 

Erb's  sign 

453 

Ouinquand's  sign 


Definition  Significance 

Loss  of  the  pupillary  reflex  to  light,  while  the  reflex  persists  with ' 
;    efforts  of  accommodation  and  the  consequent  convergence  and 
parallelism  of  eyeball  (332). 


Tabes, 
paresis 
("and 
syphilis 
(661). 


A  wavering,  staggering  and  even  falling  when  attempting  to  stand 
still  with  eyes  shut  and  with  the  feet  in  contact,  either  laterally  or 
the  one  before  the  other  (41). 

A  loss  of  the  normal  sensitiveness  to  pressure  of  the  ulnar  nerve 
behind  the  elbow. 

Pressure  on  the  nerve  trunks  of  the  extremities  causes  a  tetanic  ' 

spasm  of  the  muscles  supplied  by  them. 

I  Tetany 
The  facial  nerve  shows  extreme  irritability  to  percussion  or  pres-  f      (614). 

sure. 
Muscles  and  nerves  are  unusually  excitable  both  to  galvanism  and 

to  faradism. 


i:,i 

Erb's  paralysis 
Combined 
shoulder  and  arm 
paralysis  (490) 


Patient  spreads  his  fingers  and  presses  their  tips  against  the 
palm  of  the  observer's  hand  which  is  held  vertically. 
After  a  few  seconds  a  series  of  slight  shocks  are  felt  as  if 
the  phalanges  of  each  finger  were  knocking  together. 


I.-,:, 
Klumpke's 

paralysis 

I  190) 


A  paralysis  of  the  deltoid,  biceps,  brachialis  anticus  and  supina- ' 
tors,  long  and  short.  In  some  cases  the  supra-  and  infra- 
spinatus muscles  are  also  paralyzed,  and  to  a  less  extent  the 
extensors  of  the  wrist  and  fingers.  Anesthesia  of  outer  aspect 
of  forearm  and  hand  is  occasionally  present.  Paralysis  of 
5th  and  6th  cervical  nerve  roots. 


A  paralysis  of  the  small  muscles  of  the  hand  and  fingers.  There 
is  anesthesia  of  ulnar  side  of  forearm  and  hand.  In  some 
cases  the  muscles  of  the  forearm,  except  the  supinator  lon- 
gus,  arc  also  paralyzed,  and  the  eve  on  the  same  side  ex- 
hibits myosis,  retraction  of  the  bulb  and  narrowing  of  the 
eyelid  Opening.  Paralysis  of  nerves  arising  from  the  7th  and 
8th  cervical  anil  1st  dorsal  nerve  roots. 


Chronic 
alcohol- 
ism. 


Lesion  of 
the  brachial 
plexus. 

Erb's  paral- 
ysis. May  be 
due  to 
injury  at 
birth 
(obstetric 
paralysis   or 
I  hichenne'a 
palsy). 


166 
Brudzinski's 

neck  sign 

167 

I'.niil/in.ski's 

ign 


vVhen  the  arms  ami  le^'s  are  flexed  fully  on  the  trunk  ami  the 
head  is  passively  Lent  forward  the  patient  shows  signs  of 
pain. 

When   one  leg  is  passively  fully   Hexed  on   the  trunk   tl tlier 

drawn   up  by  the  patient    into  a  similar  position. 


•  Meningitis. 


468  Inability  of  a  patient  when  lying  on  his  hack  to  raise  both  legs  Organic 

!  and  simultaneously  although  he  is  able  to  raise  either  leg  sepa-  hemiplegia 

Qail  lately.  (incom- 

phenomenon  plete) 


115 


ANATOMICAL  TERMS 
460 
Brain  stem  Comprises  the  medulla  oblongata,  pons  varioli  and  crura  cerebri.     (Figs.  18-23.) 

461  Motor  cerebral  cortex,  corona  radiata,  internal  capsule,  pyramidal   tracts  at 
Central  motor  base  of  brain,  motor  decussation  and  crossed  and  direct  pyramidal  tracts 

neurons  (upper       in  spinal  cord.     Figs.  15-26.) 
motor  neurons) 

462  Motorial  end  plates,  peripheral  nerves,  anterior  nerve  roots,  nerve  cells  in  the 
Peripheral  motor       anterior  horns  of  spinal  cord  and  the  motor  nuclei  in  the  brain  stem.     (Figs. 

neurons  (lower        19,  26.) 
motor  neurons) 

463  Sensory  cerebral  cortex,  corona  radiata,  internal  capsule,  cerebellum  and  its 
Central  sensory  peduncles,  lemniscus  and  sensory  decussation,  nuclei  of  columns  of  Goll  and 

neurons  (upper       Burdach,  antero-lateral  ascending  (Gower's)  tract,  direct  cerebellar  (Flech- 
sensory  neurons)    sig's)  tract  and  column  of  Clark.      (Figs.  15-26.) 

464  Sensory  end  organs,  peripheral  nerves,  posterior  nerve  roots,  spinal  ganglia, 
Peripheral  sensory     posterior  horns  and  columns  of  Goll  and  Burdach  in  the  spinal  cord  and 

neurons  (lower       nuclei  of  columns  of  Goll  and  Burdach.     (Figs.  22-6.) 
sensory  neurons) 

465  Situated  in  the  lateral  horn  of  gray  matter  in  the  last  cervical  and  first  dorsal 
Cilio-spinal  center      segment  of   the  spinal  cord  and  is  connected  with  a  higher  center  in  the 

(335,  1191-2)  medulla.     Destructive  lesions  of  this  center  and  its  nerve  roots  cause  (1st) 

a  paralytic  myosis,  (2d)  a  narrowing  of  the  eyelid  opening,  (3d)  an  enoph- 
thalmus;  while  irritative  lesions  (rare)  of  this  center  and  its  nerve  roots 
cause  (1st)  a  spasmodic  mydriasis,  (2nd)  an  exophthalmus. 


116 


PART  II 


DIFFERENTIAL  DIAGNOSIS 


A  CLINICAL  DIAGNOSTIC  ANALYSIS  OF  THE  SYMPTOMS 


OBTAINED  FROM  THE  EXAMINATION   OF  PATIENTS 


117 


INTRODUCTION  TO  THE  DIAGNOSTIC  CHARTS 
DIRECTIONS  FOR  THEIR  USE 

In  using  this  book  for  diagnostic  purposes  the  student,  or  practitioner,  having  made  a  com- 
plete examination  of  the  patient  according  to  the  scheme  presented  in  chart  I,  should  make  note 
of  the  more  important  symptoms.  Then,  selecting  any  one  of  these  symptoms,  he  should  turn 
to  the  table  of  contents  and  see  which  chart  treats  of  the  disorders  which  include  this  symptom. 
Finally,  turning  to  the  commencement  of  the  chart  indicated,  he  should  apply  one  test  after 
another  until  he  reaches  the  diagnosis. 

At  the  left  margin  of  each  chart  is  placed  the  symptom  to  be  analyzed;  on  the  right  margin 
are  placed  all  the  possible  diseases  in  which  this  symptom  can  occur.  Proceeding  from  left 
to  right,  in  each  column  a  number  of  alternatives  are  offered,  and  by  selecting  the  one  appro- 
priate to  the  case  the  diagnostician  proceeds  from  one  column  to  the  next,  until  he  reaches  the 
correct  diagnosis.  In  the  column  immediately  preceding  the  diagnosis  is  an  abstract  of  most 
of  the  symptoms  which  may  occur  at  different  stages  of  the  disease.  The  great  majority,  but 
not  necessarily  all,  of  the  symptoms  given  in  the  abstract  should  be  present  in  the  history  or 
found  in  the  examination  of  the  case,  if  the  diagnosis  be  correct. 

A  few  practical  examples  will  illustrate  the  method  much  better  than  a  long  general  descrip- 
tion. Let  us  then  consider  a  few  cases  as  they  occur  in  actual  practice.  Only  the  essential 
symptoms  are  noted. 

Case  I.  Male,  aet.  51. — He  smoked  and  chewed  tobacco  and  drank  to  excess  for  years. 
About  two  months  ago  he  began  to  have  pains  at  various  points  in  both  logs.  His  legs  became 
slowly  weaker  and  his  flesh  became  tinder,  but  he  is  able  to  walk  a  mile.  Organic  reflexes 
normal.  Feet  cold,  and  the  legs  have  lately  grown  smaller.  On  physical  examination  the 
muscles  of  the  lower  legs,  and  less  so  those  of  the  thighs  are  weak,  tender  and  somewhat  atro- 
phied. The  legs,  and  especially  the  feet  show  slight  anesthesia,  marked  analgesia  and  well 
marked  retardation  of  the  conduction  of  pain.  Achilles  rellex  absent.  A  slight  knee-jerk  can 
I btained  with  difficulty.      In  walking  toes  drop  a  little  and  the  knees  are  raised  abnormally  high. 

Important  symptoms:  Pakalysis  (weakness),  HlOH-STBFFING  GAIT,  Ammiiisiv  and 
Pain. 

The  chief  symptom  in  this  case  is  weakness,  and  we,  therefore,  turn  to  chart  X,  which  dis- 
'diseasos  causing  motor  paralysis.*'  The  paresis  in  this  case  is  continuous  and  the  reflex 
acts  are  diminished  or  absent.  We,  therefore,  have  to  do  with  a  flaccid  paralysis  and  turn  to 
chart  Xa.  The  presence  of  muscular  atrophy  following  the  paralysis,  together  with  the  absence 
o|  any  apparent  hypertrophy,  guides  us  in  the  second  column  aw:iy  from  the  functional  diseases 
and  the  muscular  dystrophies  and  to  the  degenerative  atrophies;  while  the  normal  organic 
reflexes  guide  us  in  the  third  column  away  from  the  spinal  cord,  and  to  the  peripheral  tterve, 
The  presence  of  anesthesia,  pains,  muscle  tenderness  and  other  Sensor]  .-\  mptoms 
guide  us  in  the  fourth  column  to  the  class  of  neuritis  of  the  spinal  nerves.  In  the  fifth  column 
the  fact  that  there  are  many  spinal  nerves  affected  guides  us  to  the  diagnosis:  Multiple  Neuritis, 

which  the  history  of  alcoholic  abuse  confirms. 

We  can  approach  tin-  case  in  another  way  by  considering  his  abnormal  walk.     In  the  table 

of  contents  we  find  that   disorders  of  gail   are  treated  in  chart    XIII   and  indeed  in  chart    Mile 

The  walk  in  this  case  is  evidently  "paralytic  and  flaccid,"  the  tendon  reflexes  being  diminished. 

furthermore  it  is  a  high-stepping  gait,      \  comparison  of  the  three  possible  abstracts  with  the 

Symptoms  of  our  case  makes  it   evident   that   the  case  is  one  of  Multiple  Neuritis. 

We  can  trace  the  case  also  by  mean-  of  the  anesthesia  ami  analgesia:  symptoms  which  are 
ed  in  chart   \l\a.       Tin-  tendon  nllexes  being  diminished  ami  the  organic  reflexes  normal 

in  this  case,  we  are  led  to  three  &1   trai  I     onlj  one  ()f  which  fits  our  ca-e,  ami  thus  the  diagnosis 

11'." 


of  Multiple  Neuritis  is  again  confirmed.  Finally  we  may  take  up,  the  initial  symptom  in  the 
case:  pain  in  the  legs.  Pain  is  discussed  in  chart  XV  and  pain  in  the  extremities  in  chart  XVc. 
In  our  case  the  pain  is  bilateral  and  is  associated  with  anesthesia;  so  that  we  are  again  brought 
to  three  abstracts,  of  which  the  one  of  Multiple  Neuritis  most  nearly  fits  our  case. 

Case  II.  Female,  aet.  23. — Ten  years  ago  she  and  her  brother  had  simultaneously  an 
attack  of  headache,  backache  and  fever.  Her  brother  died  and  she  recovered  with  a  paralysis 
of  both  legs,  which  has  since  improved,  rapidly  at  first,  then  more  slowly.  Her  legs  are  still 
somewhat  weak,  especially  the  left  one,  but  she  can  walk  fairly  well.  No  sensory  disturbances, 
organic  reflexes  normal.  On  physical  examination  there  is  a  decided  weakness,  slight  atrophy 
and  slight  shortening  of  left  leg.  Knee-jerks  are  absent  in  both  legs.  No  objective  sensory 
abnormalities. 

Important  symptoms:     Paralysis. 

In  the  analysis  of  this  case  we  follow  the  same  path  traced  in  case  I  until  we  reach  column 
four  in  chart  Xa.  In  this  case  there  are  no  sensory  symptoms,  the  paralysis  involves  neither 
the  cranial  nor  the  extensor  nerves  exclusively,  and  is  acute  in  its  origin;  so  that  the  diagnosis 
must  be  Acute  Anterior  Poliomyelitis. 

Case  III.  Male,  aet.  48. — Had  a  chancre  followed  by  a  cutaneous  rash  twenty-two  years 
ago.  During  the  past  ten  years  has  had  "lightning  pains"  in  legs  and  a  girdle  sensation,  also 
gastric,  vesical  and  urethral  crises.  During  the  past  six  months,  his  walking  has  become  diffi- 
cult and  awkward  and  is  much  worse,  practically  impossible,  in  the  dark.  Organic  reflexes 
normal,  except  for  some  delay  in  micturition.  On  physical  examination  there  is  no  loss  of 
muscular  power,  but  all  movements  of  legs  are  awkward,  violent  and  excessive.  There  is 
marked  ataxia,  anesthesia  in  areas  and  well  marked  retardation  of  conduction  of  pain  from 
feet.  Complete  absence  of  knee-jerk.  Argyll-Robertson's  pupillary  reflex,  Romberg's  symptom 
and  loss  of  muscle  sense  in  legs.  Lumbar  puncture  gave  fluid  showing  the  presence  of  globulin 
and  lymphocytosis  and  a  positive  Wassermann.  In  walking  the  patient  does  not  stagger,  but 
flings  feet  out  widely. 

Important  symptoms:  Ataxia,  Ataxic  Gait,  Anesthesia,  Pain,  Abdominal  Crises, 
and  Lymphocytosis  in  Cerebro-spinal  Fluid. 

In  this  case  there  is  no  loss  of  motor-power  but  well  marked  ataxia  in  legs.  From  the 
table  of  contents  we  learn  that  disease  causing  perversion  of  motion,  including  ataxia,  are  treated 
in  chart  Xlla,  to  which  we  turn.  As  the  patient  does  not  stagger  in  walking  and  the  move- 
ments of  the  legs  are  ataxic,  not  only  in  walking,  but  also  in  other  movements,  it  is  certain  that 
the  case  is  one  of  "motor  ataxia."  The  ataxia  is  bilateral  and  the  knee-jerks  are  absent;  so 
that  it  is  evident  that  we  have  to  do  with  tabes  or  multiple  neuritis  (pseudo-tabes).  We  differ- 
entiate these  two  diseases  by  comparing  the  abstracts  of  their  symptoms.  As  in  this  case  there 
is  no  muscular  weakness,  atrophy  and  tenderness,  it  is  plain  that  the  diagnosis  is  Tabes. 

We  may  also  reach  a  diagnosis  in  this  case  by  studying  the  patient's  walk  with  the  aid  of 
chart  XIIIc.  The  gait  is  ataxic,  rather  incoordinated  than  staggering,  the  knee-jerks  are 
abolished  and  there  is  Argyll-Robertson's  phenomenon,  so  that  the  diagnosis  of  Tabes  is  con- 
firmed. Furthermore  we  may  trace  the  case  by  the  symptom  of  anesthesia  with  the  aid  of 
chart  XlVa.  The  tendon  reflexes  are  abolished.  The  organic  reflexes  are  not  much  disordered, 
but  they  are  slightly.  There  is  no  motor  paralysis  and  thus  we  are  led  again  to  Tabes.  If 
we  consider  the  symptom  named  "Argyll-Robertson's  phenomenon,"  which  is  present  in  this 
we  shall  find  it  discussed  in  chart  XlVd  and  here  again  we  are  led  directly  to  Tabes.  If 
we  consider  the  pains  in  the  legs  or  the  girdle  sensations  about  the  body  or  the  abdominal  crises, 
we  find  them  discussed  in  chart  XV  and  in  either  case  are  led  to  Tabes.  If  we  consider  the 
results  of  the  examination  of  the  cerebro-spinal  fluid  with  the  aid  of  chart  XIX,  we  find  the 
butyric  acid  test  positive,  the  existence  of  lymphocytosis,  a  positive  Wassermann,  a  clear  fluid 
and  ataxia,  and  thus  the  diagnosis  of  Tabes  is  again  confirmed. 

120 


Case  IV.  Female,  aet.  19. — Patient's  father  and  mother  were  first  cousins.  They  had 
eight  children,  of  whom  three  died  in  infancy  and  four  are  healthy.  Child  learned  to  walk 
late  and  with  difficulty,  frequently  stumbled  and  fell.  Was  backward  at  school  and  when  she 
was  nine  years  old  it  was  evident  to  all  that  she  was  not  normal.  Patient's  movements  became 
gradually  and  steadily  more  awkward.  Now  she  cannot  walk  without  aid.  General  move- 
ments are  slightly  ataxic  and  simulate  somewhat  a  tremor.  Movements  of  the  legs  are  more 
ataxic  and  weaker  than  those  of  the  arms.  Her  walk  is  extremely  ataxic  and  staggering.  No 
knee-jerks,  Babinski  present.  Organic  reflexes  normal.  Internal  strabismus.  No  loss  of 
muscle  sense. 

Important  symptoms:    Ataxia  and  Ataxic  Gait. 

The  most  characteristic  symptom  in  this  case  is  ataxia  and  so,  as  in  case  III,  we  turn  to 
chart  Xlla.  In  this  case,  the  ataxia  is  mainly  on  walking  and  there  is  no  motor  paralysis  and 
no  loss  of  muscle  sense.  We  are,  therefore,  brought  to  the  alternative  as  to  whether  the  disease 
occurs  in  an  adult  or  a  child.  This  case  doubtless  dates  from  early  childhood.  There  are  no 
similar  cases  among  her  brothers  and  sisters,  but  she  comes  certainly  from  a  tainted  family. 
She  lias  no  nystagmus,  but  has  strabismus.  As  this  case  began  before  puberty  and  has  no  knee- 
jerks  it  is  doubtless  a  case  of  Friedreich's  Ataxia.  The  strabismus  points  to  Marie's  hereditary 
cerebellar  disease  and  indeed  these  two  diseases  are  so  closely  related  that  there  is  some  ques- 
tion as  to  whether  they  are  separate  entities. 

We  may  approach  this  case  from  a  different  angle.  The  chief  symptom  is  difficulty  in  walk- 
ins;.  We  turn,  therefore,  to  chart  XIIc  and  note  that  the  walking  is  ataxic.  The  staggering 
gait  which  is  permanent,  the  bad  heredity,  the  absence  of  knee-jerk  and  the  commencement 
of  the  disease  in  infancy  confirms  the  diagnosis  of  Friedreich's  Ataxia.  It  may  be  noted  in 
passing  that  this  case  does  not  show  a  distinct  tremor,  or  nystagmus,  or  the  blurred  speech 
which  symptoms  are  often  present  in  this  disease. 

Case  V.  Male,  aet.  62. — His  disease  commenced  with  difficulty  in  speaking  and  swallow- 
ing about  a  year  ago,  and  has  slowly  and  steadily  progressed.  His  speech  has  become  so  bad 
that  it  is  unintelligible  and  he  has  the  greatest  difficulty  in  swallowing,  and  chokes  over  his 
food.  There  is  constant  drooling  of  saliva  from  his  mouth.  Cannot  protrude  his  tongue  beyond 
his  teeth,  cannot  raise  his  arms  because  of  weakness  of  muscles  about  the  shoulders.  His  legs 
are  somewhat  weak.  Fibrillary  contractions  and  great  atrophy  of  muscles  of  tongue  and  of 
shoulder  girdle  (deltoid,  pectorals,  etc.).  Muscles  of  hands  are  not  involved.  Absence  of 
tendon  reflexes  iii  arms.  Knee-jerks  lively,  ankle-clonus  and  Babinski  are  present.  There 
are   no   sensory   disturbances. 

Important   symptoms:     Paralysis,   Kiiuullary  Contraction    and    Muscular  Atropht. 

The  principal  symptom  in  this  case  is  a  motor  paralysis.  We  turn,  therefore,  to  chart  \. 
The  paralysis  certainly  is  a  continuous  one  and  of  the  three  alternatives  next  offered  us  we  must 
select  the  third,  inasmuch  as  we  have  a  llaccid  paralysis  with  muscular  atrophy  in  the  head  and 
arms  and  a  mild  Bpastic  paralysis  in  the  legs.  We  turn,  therefore,  to  chart  \c.  In  this  ease 
the  cranial  and  spinal  nerves  are  involved,  next  there  are  no  sensory  symptoms,  next  the  disease 
is  chronic,  and  finally  the  lips  tongue,  larynx  and  pharynx  are  involved;  consequently  the  diag- 
nosis is  Progressive  Bulbar  Paralysis.  Hut  this  diagnosis  does  not  explain  the  paralysis  and 
atrophy  of  the  muscles  of  the  shoulder  which  are  supplied  by  spinal  nerves.  We  turn,  there- 
fore,  to   the   next    sub-division,    where  spinal   nerves  are   alone   involved,  and  follow    through,   no 

■  I,  ory  symptoms  and  through  a  paralysis  involving  the  shoulder  girdle  muscles,  and  reach 

the  diagnosis  of  Amyotrophic  Lateral   Sclerosis.      The  diagnosis  is,  then,  a  combination  of  two 

diseases:   Progressive  Bulbar  Paralysis  and  Amyotrophic  Lateral  Sclerosis,  and  we  and  in  the 
abstracts  of  these  two  diseases  that  they  often  occur  together  in  combination. 

If  we  consider  the  symptom  "fibrillary  contraction'*  with  the  aid  of  chart  \llli,  it  is  evi- 
dent that  tin-  i<  an  organic  and  not  a  functional  di-i -a-e.  thai  there  is  I  marked  muscular  atrophy 
and    that    there   :)re   no  sensory    symptoms,   and   thus   the  diagnosis  of   both    Progressive    Bulbar 

Paralysis  and  Amyotrophic  Lateral  Sclerosis  is  confirmed.     Finally  if  we  consider  the  symptom 

121 


"muscular  atrophy"  with  the  aid  of  chart  XVIIa  we  find  that  the  atrophy  is  considerable  and 
of  a  relatively  rapid  course,  that  there  are  no  muscular  hypertrophy  and  no  sensory  symptoms 
and  thus  we  are  led  again  to  the  same  diagnosis. 

Case  VI.  Male,  aet.  12. — During  the  first  year  of  his  life  the  child  had  great  difficulty  in 
retaining  his  food.  At  the  end  of  his  first  year  he  began  to  have  convulsions  with  unconscious- 
ness, and  with  the  exception  of  an  interval  of  two  years  these  have  continued  up  to  the  present 
time;  the  last  attack  having  occurred  three  weeks  ago.  The  child  has  a  very  small  head  and 
an  idiotic  expression  of  face.  He  apparently  understands  most  of  what  is  said  to  him,  but  he 
can  talk  only  a  very  little  and  only  a  few  words  are  intelligible.  There  are  no  contractions  or 
deformities,  and  he  uses  his  arms  and  legs  well. 

Important  symptoms:    Anarthria  and  Idiocy. 

The  most  striking  symptom  in  this  case  is  that  a  boy  of  twelve  years  can  scarcely  speak 
intelligently.  Turning  to  the  table  of  contents  we  find  that  disorders  of  speech  are  treated  in 
chart  XIII,  to  which  we  turn.  The  loss  of  speech  in  this  case  is  so  nearly  complete  that  it  can 
be  called  anarthria,  which  is  discussed  in  chart  XHIa.  The  disease  is  evidently  congenital, 
and  the  expression  of  the  face  is  idiotic,  and  reading  and  writing  are  impossible;  so  that  the 
diagnosis  is  Idiocy.  Had  we  on  the  other  hand  decided  that  the  child  could  speak,  but  very 
imperfectly  and  unintelligibly  we  should  have  sought  for  the  disease  in  the  same  chart  XHIa, 
under  the  heading  of  dysarthria.  Here  the  congenital  nature  of  the  defect  and  the  absence  of 
cleft  palate,  etc.,  would  have  led  us  directly  to  Imbecility.  In  order  to  trace  the  case  further 
let  us  follow  the  cross  reference  after  idiocy  which  is  1081  and  which  we  find  in  chart  XVIc. 
This  case  on  account  of  his  convulsions  might  be  classed  under  Epileptic  Idiocy  or  on  account 
of  his  small  head  under  Microcephalic  Idiocy,  or  under  both. 

Case  VII.  Female,  aet.  53. — Complains  of  trembling  and  that  she  cannot  execute  any 
movements  quickly,  because  her  arms  and  legs  are  stiff  and  rigid.  When  walking  she  has  a 
decided  tendency  to  pitch  forward.  Feels  warm  at  times  when  the  room  seems  cool  to  others. 
Expressionless  face,  passive  tremor  of  hands.  Propulsion  and  retropulsion  when  walking  or 
standing.  Rigidity  of  arms  and  legs.  Difficulty  in  rising  from  a  low  chair.  Knee-jerks  rather 
increased. 

Important  symptoms.:    Muscular  Rigidity,  Tremor  and  Abnormal  Walk. 

The  most  characteristic  symptom  in  this  case  is  the  rigidity  of  the  arms  and  legs  which  is 
a  mild  tonic  spasm.  From  the  table  of  contents  we  learn  that  diseases  causing  spasm  are 
treated  in  chart  XI,  to  which  we  turn  and  find  that  general  tonic  spasm  is  discussed  in  chart  Xlb. 
In  this  case  there  is  no  fever  and  of  the  five  sub-divisions  under  this  head,  this  case  clearly  falls 
in  the  second:  "rigidity  which  does  not  prevent  passive  or  voluntary  motions."  Of  the  two 
alternatives  next  offered  it  is  evident  that  we  must  choose  the  second,  in  the  abstract  of  which 
we  find  all  the  symptoms  present  in  our  case.    The  diagnosis  is,  therefore,  Paralysis  Agitans. 

If  we  follow  the  symptom  "tremor,"  we  find  this  treated  in  chart  Xllb.  It  is  a  passive 
tremor  and,  whether  it  be  increased  or  diminished  on  voluntary  movements,  if  it  be  slow,  the 
abstracts  show  that  it  is  a  case  of  Paralysis  Agitans,  because  the  other  abstracts  do  not  fit  this 
case  at  all. 

If  we  consider  the  difficulty  in  walking  in  this  case  we  turn  to  chart  XIIIc.  In  the  three 
great  divisions  offered  this  case  evidently  falls  in  the  third:  "paralytic  and  spastic;"  and  of 
the  two  sub-divisions  next  offered  we  must  take  "general  rigidity"  which  leads  us  again  to 
the  diagnosis  of  Paralysis  Agitans. 

Case  VIII.  Male,  aet.  59. — During  the  past  34  years  has  had  at  times  attacks  of  asthma. 
During  the  past  four  years  has  been  troubled  by  a  great  many  paroxysmal  attacks  of  vertigo, 
at  irregular  intervals;  some  are  slight,  some  are  so  severe  as  to  throw  him  from  a  chair  half  way 
across  the  room  to  the  floor,  where  he  must  lie  for  several  hours,  because  when  he  raises  his  head 
from  the  floor  he  vomits  violently  and  the  dizziness  becomes  worse.  He  often  has  slight  attacks 
of  vertigo,  which  make  him  stagger  when  walking.     During  these  four  years  he  has  been  slowly 

122 


growing  deaf  in  his  left  ear;  the  deafness  being  now  extreme.  He  has  also  had  during  the  same 
time  in  the  same  ear,  a  buzzing  and  a  ringing  which  is  most  intense  just  before  an  attack  of 
vertigo.  He  has  no  paralysis  and  no  loss  of  muscle  sense.  Bone  conduction  is  absent.  He 
also  is  much  troubled  by  gastric  flatulence,  to  which  he  attributes  his  vertigo,  but  when  he  takes 
digestive  medicine  and  the  digestive  disturbances  are  relieved,  the  vertigo  remains  unchanged. 
His  eyes  were  found  to  be  astigmatic  and  proper  glasses  used,  but  no  improvement  in  the  attacks 
of  vertigo  followed. 

Three  years  after  the  above  record  was  made  the  attacks  were  milder  and  less  frequent, 
but  at  that  time  his  left  ear  was  totally  deaf  and  deafness  was  advancing  in  his  right  ear. 

Important  symptoms:    Paroxysmal  Vertigo,  Staggering  Walk  and  Deafness. 

In  this  case  the  principal  symptom  is  paroxysmal  attacks  of  vertigo;  diseases  causing  which, 
we  learn,  are  treated  in  chart  XVd.  We  see  from  this  chart  that  vertigo  may  be  caused  by 
digestive  disturbances  and  disease  of  the  eye,  both  of  which  were  present  in  this  case,  but  the 
vertigo  persisted  when  these  abnormal  conditions  were  relieved;  so  that  they  could  hardly  be 
the  cause.  On  the  other  hand,  we  find  that  vertigo  is  associated  with  deafness:  a  prominent 
symptom  in  this  case,  and  in  looking  over  the  abstract  of  this  form  of  vertigo  we  see  that  it 
fits  the  case  exactly;  so  that  the  diagnosis  is  Meniere's  Disease. 

If  we  consider  another  symptom  "the  occasional  staggering  in  walking,"  we  find  this  treated 
in  chart  Xlla.  This  patient  has  no  loss  of  muscle  sense  and  no  muscular  paralysis.  He  is 
an  adult  and  his  hearing  is  abnormal  and  thus  we  are  led  again  to  Meniere's  Disease.  Finally 
if  we  trace  the  symptom  "deafness"  with  the  aid  of  chart  XlVe  we  find  that  the  deafness,  at  any 
rate  at  first,  was  unilateral,  that  bone  conduction  is  absent,  that  there  is  no  facial  paralysis  and 
that  severe  paroxysmal  vertigo  and  tinnitus  aurium  is  present;  thus  confirming  again  the  diagn.  Pl- 
ease IX.  Female,  act.  17. — Heredity  good.  Was  well  until  about  three  years  ago  when. 
at  the  time  of  commencing  menstruation,  she  began  to  have  attacks  of  clonic  convulsions  with 
unconsciousness,  which  have  continued  up  to  the  present  time  and  in  which  she  has  occasionally 
bitten  her  tongue.  Has  also  lesser  attacks  of  unconsciousness,  or  very  cloudy  consciousness 
in  which  she  automatically  prays,  or  says  foolish  things.  Has  no  memory  of  any  of  her  attacks. 
She  has  an  immediate  aura  of  fire  before  her  eyes  and  of  wheels  revolving  in  her  head.  Some 
headache  follows  the  attack.  The  convulsions  occur  only,  and  the  lesser  attacks  mainly,  at 
night.  Physical  examination  is  negative,  urine  normal.  Fundus  of  eye  normal.  Knee- jerks 
equal.    Much  acne  on  face. 

Important  symptoms:    Coma  and  Convulsions. 

The  constant  symptom  in  all  her  attacks  is  unconsciousness,  or  coma,  of  short  duration. 
This  symptom  is  treated  in  chart  \\  la.  There  is  HO  history  of  recent  injury,  of  brain  dise.'i-e. 
of  poisoning,  of  heart   disease,  of  paralysis,  of  kidney  disease  or  of  fever.      Therefore,   we  are 

led  at  once  to  the  diagnosis  of  Epilepsy  or  of  Eclampsia     The  latter  can  be  excluded  by  the 

frequently  recurring  attacks  at   long  intervals. 

If  we  next  take  the  symptom  of  clonic  convulsion  with  the  aid  of  chart  XIa.  we  find  that 
there  is  no  fever  and  the  convulsion  is  a  universal  one,  and  not  local  at  the  onset.  There  is 
coma  and  there  are  no  symptoms  of  disease  of  the  brain  or  cord,  or  of  the  kidnc\  -.  heart  Ot 
Mood,  or  of  poisoning  and   thus  we  confirm   the  diagnosis  of   Kpilepsy. 

Case  \.      female,  act.  84.      Nine  years  ago  one  morning,  her  left  arm.  lei;  ami  side  of  lace 

felt  numb  and  -Ic  could  not  see  things  on  her  left  >ide  without  turning  her  head.  These  symp- 
toms steadily  increased  during  the  day  and  she  could  not    use  her  leg,  and  especially  her  arm. 

well.     She  could  always  walk,  but  at  first  she  could  walk  only  with  difficulty.     This  difficulty 

in  walking  gradually  passed  away.  She  could  use  her  arm.  but  could  not  use  it  well  for  more 
than  a  year,  and  it  is  not  quite  righl  even  at  the  present  lime.  The  numbness  of  the  left  side 
and  the  inability  to  see  things  on  her  left  still  persist.  (In  physical  examination  there  is  found 
anesthesia   and  analgesia  of  the   left    arm   and   leg  and  of  left  side  of  body  and  face,  (left    heini 

anesthesia  and  hemianalgesia),  also  blindness  in  each  eye  for  all  objects  to  the  left  of  oentral 

128 


vision  (left  homonymous  hemianopia).  The  left  arm  and  leg  are  a  little  awkward  and  a  trifle 
weak;  strength  of  left  hand  grasp  to  that  of  right  is  as  80  to  105.  Knee-jerks  lively,  perhaps 
stronger  on  left  side:  neither  ankle-clonus  nor  Bahinski.     Organic  reflexes  normal. 

Important  symptoms:     Hemianesthesia,  Hemianalgesia  and  Homonymous  Hemianopia. 

The  principal  symptoms  of  this  case  are  hemianesthesia,  hemianalgesia  and  homonymous 
hemianopia.  These  are  sensory  symptoms  and  indeed  symptoms  of  a  diminution  of  sensation. 
We  turn  to  the  table  of  contents  and  find  that  "diseases  causing  a  diminution  of  sensation" 
are  considered  in  chart  XIV,  which  we  next  consult.  Starting  with  disorders  of  sensation  in 
the  first  column,  we  have  five  alternatives  offered  us  in  the  second  column,  among  which  we 
ought,  without  doubt,  in  this  case  to  select  diminution  of  sensation  and  following  this  division 
we  have  in  the  next  column  three  alternatives,  among  which,  undoubtedly,  we  should  select 
anesthesia  and  analgesia  and  turn  to  chart  XlVa.  In  this  chart  we  have  the  alternatives  of 
the  tendon  reflexes  being  either  absent  or  present.  In  the  above  case  they  are  present.  The 
dilemma  in  the  next  column  is  quickly  decided  because  the  organic  reflexes  are  normal.  The 
history  of  a  motor  paralysis  lasting  a  year  or  more  and  still  slightly  persisting  directs  us  to 
the  first  alternative  in  the  next  column,  especially  as  there  are  no  hysterical  symptoms  present; 
while  the  unilateral  nature  of  the  symptoms  and  next  the  acute  onset  (one  day)  brings  us  to 
the  diagnosis  of  Cerebral  Hemorrhage  or  Softening. 

To  determine  which  lesion  is  present,  we  follow  the  first  cross  reference,  No.  503-6,  which 
we  find  in  chart  Xb.  In  looking  over  the  abstracts  differentiating  cerebral  hemorrhage,  embol- 
ism and  thrombosis,  our  case,  with  its  relatively  slow  onset,  its  absence  of  any  coma,  its  absence 
of  any  source  for  an  embolism,  is  probably  one  of  cerebral  thrombosis  and  certainly  one  of  cere- 
bral apoplexy. 

The  next  question  is  as  to  the  locality  of  the  softening.  To  ascertain  this  we  turn  to  the 
table  of  contents  and  find  that  "localization  from  symptoms  of  paralysis"  is  discussed  in  chart 
XXII  to  which  we  turn.  The  reflexes  being  present  in  our  case,  we  are  brought  to  the  ques- 
tion whether  sensory  or  motor  paralysis  is  dominant.  In  our  case  sensory  paralysis  is  dominant 
and  we  turn  to  chart  XXIIc.  Of  the  first  alternative  offered  us  in  this  chart  we  must  choose 
the  first:  anesthesia  and  analgesia.  In  regard  to  the  next  column,  the  distribution  of  the  anes- 
thesia in  our  case  evidently  falls  into  the  class:  "the  (left)  arm,  leg  and  face  are  anesthetic." 
In  our  case  there  is  no  Jacksonian  epilepsy  and  there  is  hemianopia,  so  that  the  localization  of 
the  softening  is  in  the  posterior  part  of  the  right  internal  capsule.  If  we  now  turn  to  fig.  17 
we  can  easily  see  how  a  lesion  in  the  posterior  portion  of  the  internal  capsule  can  easily  involve 
the  sensory  fibers  from  one-half  the  body  and  also  the  optic  fibers;  the  continuation  of  the  optic 
tract.  It  is  also  easy  to  understand  that  on  account  of  the  wide-spread  circulatory  disturbances 
in  the  early  stages  of  the  disease,  before  a  collateral  circulation  had  to  a  degree  reestablished 
itself  in  the  periphery  of  the  lesion,  the  motor  fibers  lying  directly  anterior  should  be  involved 
and  a  more  or  less  temporary  hemiplegia  should  occur,  as  was  indeed  the  case.  It  seems  strange 
that  deafness  did  not  occur  in  this  case  as  it  is  certain  that  the  auditory  fibers  also  must  have 
been  involved  in  the  lesion,  but  it  is  well  known  that  central  lesions  only  produce  deafness,  even 
unilateral  deafness,  when  the  lesion  is  bilateral  (see  page  8). 

Thus  we  have  arrived  by  means  of  the  charts  to  the  diagnosis  of  this  case  of  "thrombosis 
oi  the  artery  supplying  the  posterior  portion  of  the  internal  capsule,"  but  in  order  to  make  this 
diagnosis  doubly  sure,  let  us  take  another  one  of  the  prominent  symptoms,  such  as  homonymous 
hemianopia,  and  follow  it  through  the  charts.  This  symptom  is  also  a  diminution  of  sensa- 
tion and  therefore  we  turn  again  to  chart  XIV.  Disregarding  this  time  diminution  of  sensa- 
tion we  follow  "disturbances  of  vision"  and  "limitation  of  field  of  vision"  to  chart  XlVb.  Here 
we  find  homonymous  hemianopia  and  in  the  next  column  there  can  be  no  doubt  that  we  must 
choose  the  path  which  hemianesthesia  indicates  and  by  it  are  led  to  the  diagnosis  of  hemorrhage, 
or  softening,  in  the  posterior  part  of  the  posterior  limb  of  the  opposite  sided  internal  capsule, 
which  is  the  diagnosis  to  which  we  had  already  reached  by  another  road. 


124 


CHART  X 


Motor  Paralysis 

DIAGNOSTIC  ANALYSIS  OF  SYMPTOMS. 

Tests 


Symptoms 
Analyzed 


Permanence  Reflexes  in  Paralyzed  Muscles 

of  Paralysis 

'Abolition  or  diminution  of  both 
voluntary  and  reflex  acts  in  the 
muscles  involved. 

472 


469 

MOTOR  PAR- 
ALYSIS OR 
PARKS  IS 
(244) 

After  aoarefol  ex- 
amination has 

shown  that 
the  paralysis 

is  a  true  one 
and  is  not 
simulated  by 
any  ankylosis 

or  by  pain  on 

motion. 


470 

CONTINUOUS 
PARALYSIS 


171 

INTER- 
Ml  [TENT 
PARALYSIS. 


FLACCID  PARALYSIS  (252) 

Lesions  of  peripheral  motor  neu- 
rons. 

There  are  hypotonia  and  changes 
in  the  electrical  reaction  of  the 
nerves  and  muscles  involved  in 
very  varying  degree  from  simple 
diminution  in  excitability,  to 
complete  reaction  of  degenera- 
tion. 


Abolition  or  diminution  of  volun- 
tary, with  persistence  or  even 
exaggeration  of  reflex,  acts  in 
the  muscles  involved. 

473 

SPASTIC  PARALYSIS  (251) 

lesions  of  central  motor  neurons. 

There  is  hypertonia  without  altera- 
tions of  electrical  reaction  of  the 
nerves  and  muscles. 


■171 

A  combination  of  FLACCID  PAR- 
ALYSIS in  the  upper  part  of  the 
paralyzed  area,  and  of  SPASTIC 

PARALYSIS  in  the  lower  part. 


All  the  muscles  of  the  body  and  ■ 
head. 

The    mUSOleS   Of   one   or    both    leps. 

rarely  of  arms. 

Commencing  in   legs,  extending  to 

arms 

ted   With  a  cervical  ril «. 
125 


The  differential  diag- 
nosis of  those  dis- 
eases in  which 
FLACCID  PARAL- 
YSIS occurs  is  set 
forth  in 
CHART  X  a. 


The  differential  diag- 
nosis of  those  dis- 
eases in  which 
SPASTIC  PARAL- 
YSIS occurs  is  set 
forth  in 
CHART  X  b. 


The  differentia]  diag- 
nosis Of  those  dis- 
eases in  which    there 

is  a  combination  of 
l  l  \ccil>  and  of 
SPASTIC    PARAI 
Ysis.  and  of  those 
In    which    INTER- 
MITTENT I'M:  LL 

YSIS    occurs 
forth  in 

ni  \i;t  \  o. 


CHART  Xa 

Flaccid  Paralysis 

Comprising  Numbers  475  to  477  on  left  side  of  Chart 
and  482  to  500  on  right  margin 


I-'". 


DIAGNOSTIC  SYMPTOMS  AND  TESTS 


47.", 
No  muscular  atro- 
1'hy,  except  rarely 
in  chrome  cases. 
Reflexes  may  be 
diminished  only, 
not  abolished. 


("Paralysis  beginning 
I  in  the  feet  and  as- 
|  rending  to  the  head 
I  in  adults. 


No    true    paralysis 
great    hy]  ' 
in  infants. 


iXO 

I  but    great    hypoto- 
nia i 


rThe  organic  r  flexes 
a  r  e  permanently 
disordered    (I    and 


47U 
Muscular  atrophy, 
usually  great,  fol- 
lowing the  paralysis 
after  the  second 
week  of  the  disease. 

Paralysis  primary. 

The     Degenerative 
Atrophies.         (See 
also  .Syringomyelia 
552,  837-3.) 


The  organic  reflexes 
are  normal  or  show  " 
only  transitory  dis- 
turbances    (1     and 
323-4), 


'I  he  paralysis  is  in  the  form  of  a  paraplegia,  commencing  in  the  feet  aj 
ing   bulbar   symptoms    (434),    and  causing  death  usually  in  the  seconc 
are   pronounced   the   disease  is  probably  a  neuritis  (488).     The  spleen  , 
dry's  paralysis  and  in  addition  hematoporphyrinuria.     (Compare  caret 

Occurs  usually  congenitally,  rarely  during  the  first  year  of  life.  No  he 
in  very  abnormal  positions.  The  child  cannot  use  the  Blight  powei 
nuts,  no  disturbances  of  organic  reflexes.    Electrical  reaction  much  c" 

rVery  acute  onset.    Sympton 
Marked  sensory  symptoms,  such  as  pain,  |      thesia.    May  be  blood  in  ci 
paresthesiae,  anesthesia,  etc.,  are  pro-  i  .  ,  ,        . 

senl    with  the  motor  symptoms.     The     Ac"'°'  sub-acute  or  dm.,,,,,  , 
legs   only   are    paralysed   and   exhibit!     °wier  evidence  of  syphilis  i 
trophic  disturbances.     There  is  incon-1  Very  chronic  and  progressive 
tinence    of   urine   and    the    bladder    is 
empty  or  nearly  so.  Very  acute,  acute  or  sub-acu 

I     of  the  cord.    Fibrillation  < 

[      perineum,  genitals  and  moj 

There  is  usually  a  history  of 
acute,   sub-acute  and  elm 
'Many   spinal    (very  and  arms  (long  neurons)  I 

'Sensory  symptoms,  rarely  cerebral)  weakness,  atrophy  and  tei 
such  as  pain,  nerve  nerves  are  affected.  duction  of  pain  and  loss  o 
and  muscle  tender-  form  of  Korsakow's  psycl 

ness,     paresthesiae,  form  rarely  runs  an  acute 

anesthesia,  etc.,  are  J  ical  form  exhibits  many  s. 

present.  The      motor      and 

The  paralysis  is  CO-  sensoiy  paralysis 
In  very  exceptional  incident  with  the  (anesthesia)  may 
cases  sensory  symp-  distribution  of  one,  be  slight  and  the 
toms  may  be  prac-  rarely  of  a  few  spi-  pain  great.  The 
tic-ally  absent,  [nal  nerves.  motor  paralysis   is 

usually         greater 

than  the  sensory. 

Occurs  must  commonly  in  inj 

For  special  forms  of  neurits 


No  Sensory  symp- 
toms, except  rarely 
pain  and  tender- 
ness over  the  nerve 
trunks  in  early 
stage. 


The  paralysis  is  co- 
incident with  the 
distribution  of  one, 
rarely  of  a  few  spi- 
nal nerves. 

■The  paralysis  is 
confined  to  the  dis- 
tribution of  one 
or  more  cranial 
nerves. 

Extensor  muscles 
are  alone   affected. 

A  paralysis  of  acute 
onset,  usually  con- 
fined to  the  arms 
and  legs,  geneially 
to  a  portion  of  one 
or  both;  in  rare 
cases  involves  the 
cranial  nerves. 

\  chronic  form, 
may  occur  exceed- 
ingly rarely. 


Nerve 

Atn 

The  rr 

ban 

1 <  Ine  o 


The  paralysis  is  usual)}   mon 

Usually  confined  to  the  extei 
lead  poisoning.    Previous 

The  paralysis  (which  is  alwa\ 

sinus.  Rarely  there  is  sligi 
so  in  children.  The  pararj 
In  infants  ami  young  chil 
neuritis  with  predominate 
turns  are  common  and  thi 

of  functionally    related   mu 

Tin-  muscles  of  I  In-  |  runi 

and  scurvy  (  Barlow's   disc. 
(4)  encephalitic  form,   (5) 
CI  i  ionic  atrophic  paralysis  (." 
i(  lompare  carefully  with   lv 

A  paralysis  of  chronic  onset  commencing  The  di: 
in  peronei  muscles  and  extending  sym-  mucl 
metrically.       Intrinsic    muscles    of    the  app 

feel   affected.  .nil 


177 
A    combination    of 

muscular     atrophy 

and    apparent    hy- 
pertrophy. 

Paralysis         secon- 
dary. 

The  Muscular  Dys- 


A  chronic  disease  commencing  in  childhood  or  youth  and  usually  showing 
marked  heredity,  It  exhibits  a  progressive  muscular  atrophy,  usually 
Combined  with  some  hypertrophy,  hence  called  muscular  dystrophy.  In 
time  all  the  muscles  become  atrophied.  The  organic  reflexes  arc  normal 
and  there  are  no  sensory  symptoms  whatever  and  no  motor  paralysis, 
except  such  as  would  result  from  the  muscular  degeneration,  Even  the  ap- 
parently hyperl  lophied  muscles  are  weak.  Tendon  reflexes  are  early  much 
diminished  and  finally  absent   in    the  affected  muscles.     There  are  no  liluil- 

lary  contractions.  The  course  of  the  disease  is  progressive,  but  very  chronic, 
lasting  many  years,  from  iis  point  of  commencement  i he  atrophy  ex- 
tends ii igboul   the  body.     It  produces  a  marked  lordosis.     Although 

the  muscular  dystrophies  are  divided  into  three  groups,  there  are  many 
transitional  and  mixed  tonus,  and  the  examination  of  the  excised  muscles 
also  shows  mixed  forms. 


The  disease  is  i 
extremities, 
muscles   shov 
wilh  a  mixti 
trophy  in  di! 

eni  parti  of  i 
More  or  less 

The  disease,  is  i 
Inanities.  E: 
cles  shows  de 
mixture  of  a 
and  especial! 
tcrstitial  fat. 


DIAGNOSTIC  ANALYSIS  OF  SYMPTOMS 
ABSTRACT  OF  SYMPTOMS 


DIAGNOSIS 


■  ascending  the  legs  and  body.    Before  the  legs  are  completely  paralysed  the  paralysis  appears  in  the  hands  and  rapidly  ascends  the  arms.    The  ascending  paralysis  reaches  the  medulla  and  pons;  produc-     Acute  Ascending  (Landry's)  Paralysis, 
ough  some  rare  cases  may  recover.    The  organic  reflexes  are  usually  normal,  except  as  affected  by  weakness  of  the  abdominal  muscles.    There  is  little  pain  and  little  or  no  anesthesia.    If  sensory  symptoms 

enlarged.    There  is  rarely  fever,  and  no  electrical  reaction  of  degeneration  (3991      Certain  drugs   especially  the  prolonged  use  of  trional  or  sulfonal,  may  cause  symptoms  closely  resembling  those  of  Lan- 

4SS  and  495.) 

luscles  exhibit  extreme  want  of  tone  and  flabbiness.    The  legs  are  always,  the  arms  are  often,  affected  but  in  less  degree.    The  mobility  of  the  joints  is  greatly  increased  and  the  extremities  can  be  placed     Myatonia  Congenita.     Amyotonia  Congenita. 
ary  muscular  contraction  still  remaining  to  any  advantage.    The  child  can  neither  sit,  stand,  nor  walk  without  assistance.    Tendon  reflexes  absent,  no  muscular  atrophy,  no  fibrillation,  no  sensory  disturb- 
but  no  reaction  of  degeneration.    The  tendency  of  the  disease  is  towards  improvement,  but  not  to  complete  recovery. 


days  and  may  improve  later.     May  be  deformity  in  lo 


of  the  vertebral  column.    The  anesthesia  always  present  is  not  preceded  by  hyperes- 
not  preceded  by  hyperesthesia.    A  history  or 


'  Injury  of,  or  hemorrhage  i 


Lumbar  en 
ment  of  spina! 
(Figs.  24-7.) 


ymptoms  continue  to  extend  for  some  time  and  are  fairly  symmetrical.     Fibrillation  may  bo  present.    The  anesthesia  usually  present 
often  found  in  syphilitic  myelomalacia  (1211)  which  is  not  as  frequent  in  the  lumbar  enlargement  as  it  is  higher  in  the  spinal  cord. 
Symptoms  at  first  mainly  unilateral,  becoming  bilateral  later.     Cerebro-spinal  fluid  is  usually  under  increased  tension. 

usually  sub-acute.  Much  pain  in  perineum  and  genitals.  May  be  deformity  in  lumbar  region  of  spine.  Bed-sores  are  less  common  and  symptoms  less  symmetrical  than  in  lesions 
n  the  peronei  muscles.  When  the  lesion  is  low  down  the  muscles  on  anterior  aspect  of  thigh  are  not  paralysed  and  knee-jerks  are  normal.  The  anesthesia  always  present  in  the 
extensively  over  legs,  is  often  preceded  by  hyperesthesia. 

alcohol,  etc.)  or  infection  (diphtheria,  etc.).  The  paralysis  is  usually  in  the  'form  of  a  paraplegia  and  increases  in  intensity  during  the  first  few  weeks,  but  in  some  cases  reaches  its  height  in  a  few  days; 
s.  The  extensors  are  usually  weaker  than  the  flexors  and  the  consequent  foot-drop  causes,  when  walking  is  possible,  a  high  stepping  gait.  The  paralysis  commences  at  the  distal  extremity  of  the  legs 
ids  towards  and  often  involves  those  of  the  body.  The  cranial  nerves  are  rarely  affected  and  then  especially  the  long  ones  (phrenic,  pneumogastric,  facial,  etc.).  The  most  characteristic  symptoms  are 
of  the  muscles  affected,  at  first  the  small  muscles  of  the  hands  and  soles  of  the  feet.  In  addition,  there  are  usually  pain,  paresthesiae,  mixture  of  hyperesthesia  and  anesthesia,  ataxia,  retardation  of  con- 
sense.  Edema  and  trophic  disturbances  are  common.  The  atrophy  and  emaciation  are  often  extreme.  Not  infrequently  there  is  fever,  and  in  alcoholic  cases  there  are  mental  disturbances  usually  in  the 
'0).  No  globulin  or  leucocytosis  in  cerebro-spinal  fluid.  Great  variations  in  type  occur.  Some  cases  may  be  purely  motor  (diphtheria,  etc.),  others  mainly  sensory  and  others  mainly  ataxic.  This  last 
''  acute  ataxia."  The  diphtheritic  form  may  involve  the  muscles  of  Ihe  extremities,  but  it  always  first  appears  in,  and  is  usually  limited  to,  the  uvular  and  ciliary  (accommodation)  muscles.  The  arsen- 
sory  disturbances  and  a  peculiar  bronzing  or  pigmentation  of  the  skin.     (Compare  carefully  with  482  and  495.) 

*  when  it  can  be  felt  and  is  usually  the  seat  of  various  paresthesiae  and  of  intense  pain.  In  severe  cases  a  complete,  or  partial,  electrical  reaction  of  degeneration  and  trophic  disturbances  are  present. 
lie  muscles  involved  and  subsequent  active  or  passive  contractures  of  the  antagonists  may  occur.     For  description  of  special  forms  of  neuritis  or  injury,  see  Chart  XII  c. 

sensory  symptoms  coincide  with  the  area  of  distribution  of  one  or  more  nerves  entering  into  the  brachial  plexus.     Muscles  of  shoulder  and  upper  arm,  5th  and  6th  cervical  (Erb's  paralysis);  or  muscles  of 
earm  with  oculo-motor  symptoms  at  times,  7ih  and  Sth  cervical  and  1st  dorsal  nerves  (Klumpke's  paralysis,  454-5)). 
nder  tumors  can  be  felt  on  one  or  on  many  nerves,  which  are  usually  the  seat  of  paresthesiae  and  of  more  or  less  pain,  often  severe. 

tsure  to  cold,  extension  of  inflammation,  syphilis  and  tumor  at  base  of  br; 
y  see  Chart  XII  c. 


The  paralysis  is  not  accompanied  by  symptoms  of  centrai  disease.   All  the  muscles  supplied  by  the  nerve  are  usually  paralysed. 


ead  and  accompanied  by  other  symptoms  of  central  disease.     Only  a  portion  of  the  muscles  supplied  by  the  nucleus  may  be  paralysed.    May  be  : 


'in  ted  with  atheromatous  arteries  or  infectii 


he  wrist  and  fingers  causing  wrist -drop.     Supinato 
lead  colic,  arthralgia,  etc.    Lead  can  be  detected  i 


the 


i  not  involved  (716).     Rarely  the  muscles  of  dorsal  flex 
rine  after  the  administration  of  iodide  of  potassium. 


olved,  causing  foot-drop.    Blue  line  on  gums.    History  of  exposure  to 


motor  and  never  sensory,  except  temporarily  in  the  legs  in  very  rare  eases) 
and  muscle  tenderness.  Lymphocytosis  and  globulin  in  cerebro-spinal  fluid 
itest  during  the  first  week  or  two  and  may  improve  rapidly  at  first  and  late: 
parts  may  remain  more  or  less  undeveloped.  The  vast  majority  of  cases  o- 
symptoms.     Deformities,   contractures,   subluxation  of  joints  from  relaxed 


lay  rarely  come  on  abruptly,  but  is  usually  preceded  by  fever  and  signs  of  meningeal  irritation,  exceptionally  even  conyi.il- 
the  acute  stage.  In  a  small  percentage  of  cases  the  disease  rapidly  terminates  fatally.  The  onset  is  always  acute,  especially 
lore  slowly,  but  recovery  is  usually  only  partial;  some  or  many  muscles  remaining  paralysed  and  atrophied  throughout  life. 
,r  in  the  first  three  years  of  life,  but  the  disease  may  occur  in  adults  and  then  may,  in  rare  cases,  closely  resemble  multiple 
contractured  muscles  and  ligaments,  and  arrest  of  growth  are  common  in  young  children.  Trophic  and  vaso-motor  symp- 
atrophy  is  usually  extreme.     The  paralysed  parts  are  usually  cold  and  cyanotic,  and  the  paralysed  muscles  exhibit  the  reaction  of  degeneration.     The  paralysis  may  have  any  distribution,  but  groups 

always  affected.     The  more  widespread  the   paralysis,  the  greater  will  probably  be  the  improvement.     The  legs  are  more  frequently  affected  than  the  arms  and  the  extensors  more  than  the  flexors. 

l  paralysed.  Cranial  nerves  rarely  affected  (acute  encephalitis).  An  infectious  disease  which  may  occur  in  epidemics,  especially  in  warm  weather.  In  young  children  the  gums  must  be  carefully  examined 
be  carefully  excluded.     Poliomyelitis  lias  been  divided  into  a  number  of  different  forms  which  are  partially  described  by  their  names  (1)  spinal  form,  (2)  Landry's  paralysis  form,  (3)  brain-stem  form, 

•ebellar  form,  (6)  neuritic  form,  in  which  form  slight  muscle  tenderness  may  occur,  (7)  meningitic  form,  (8)  abortive  form.     Some  cases  of  porencephaly  (501.)  may  have  the  same  etiology   and  pathogenesis. 

possibly  be  regarded  as  a  chronic  form  of  this  disease  with  a  very  different  etiology  and  pathology.    Whether  there  is  a  true  chronic  anterior  poliomyelitis  is  very  doubtful.    If  it  exists  it  is  certainly  very  rare. 

ally  commences  before  the  age  of  twenty  years  and  was  formerly  considered  one  of  the  muscular  dystrophies  as  there  is  often  a  well  marked  heredity.  Usually  the  paralysis  and  atrophy  do  not  extend 
:he  knees.  In  the  later  stages  of  some  rare  cases  symptoms  of  atrophic  paralysis  have  developed  in  the  hands  and  arms.  The  muscles  obtained  by  harpooning  show  simple  degenerative  atrophy,  and  no 
tertrophy.  In  rare  cases  there  may  be  pain.  Fibrillary  contractions  and  reaction  of  degeneration  are  present.  Club-foot  is  common.  Leyden  has  described  a  form  of  hereditary  muscular  atrophy  with- 
}hy,  attacking  the  legs  in  the  first  ten  years  of  life,  in  which  the  atrophy  involves  especially  the  muscles  attached  to  the  pelvis. 


■ked  in  the  upper 
ation  of  excised 
aration  of  fibers 
:ophy  and  hyper-  "* 
iers  and  in  differ- 
degenerated  fiber, 
ial  fat  is  present. 

rked  in  lower  ex- 
Dn  of  excised  mus- 
m  of  fibers  with  a 
and  hypertrophy, 
quantities   of   in- 


The  disease  usually  commences  between  the  ages  of  15  and  35  years.  The  atrophy  begins  in  the  orbicularis  oris  and  extends  to  the  other  muscles  of  the  face,  to  the  shoulder  girdle 
and  finally  to  the  legs.  Patient  cannot  whistle,  nor  speak  well,  nor  drink  easily.  Lips  are  thin  and  protrude:  "  tapir  mouth."  When  smiling  the  mouth  elongates  only,  its  corners 
are  not  raised.    Some  muscles  of  shoulder  are  often  apparently  hypertrophied  at  first  and  later  atrophied,  or  may  be  atrophied  from  the  start. 


'he  disease  usually 
especially  the  triceps 


between  the  ages  of  12  and  15  years.    The  pectorals,  trapezoid,  deltoid,  etc.,  are  often  hypert.ro phied  at  first  and  later  atrophied.     The  biceps  and 
atrophied  from  the  start.     Motion  of  shoulder  and  arm  much  impaired.    The  face  muscles  are  not  involved  until  late  in  the  disease,  if  at  all. 


The  disease  usually  commences  between  the  ages  of  2  and  7  years,  but  sometimes  much  later.  The  calf  muscles  first  showr  apparent  hypertrophy,  followed  by  the  extensor  cruri 
infra-spinati,  deltoid,  etc.  Other  muscles  are  atrophied.  AH  muscles  finally  become  atrophied.  Even  hypertrophied  nrascles  are  weak,  but  not  so  weak  as  those  which  are  atr 
phied.  Marked  lordosis  and  weakness  of  serratus  magnus  muscle.  In  rising  from  the  ground  patient  has  to  push  himsfelf  up  with  his  arms  and  crawl  up  upon  himself.  Waddlir 
gait.     Deformities  and  contractures  occur  in  the  later  stages  and  the  lordosis  is  later  replaced  by  a  marked  kyphos' 


■ute  or  chronic  myelitis  or  myelo 
S25,  1148a,  1309). 
imor  in,  or  compressing 


lalacia  of  (791, 


L  Tumor  in,  or  compressing,  (826,  1309). 
Lesions  of  the  cauda-equina  (1007,  130S).    (Fij 


Multiple    Neuritis.       Polyneuritis.       Pseudo-tabes. 
(662,  787,  823,  100S,  1147,  1307).     (Figs.  33,  38). 


Neuritis  or  injury  of  a  spinal  nerve  (sciatica,  etc.), 
(822,  941,  1146-7,  1173,  1303-5-7).  (Figs.  33,  3S). 
Neuritis  or  injury  or  tumor  of  brachial  plexus  \  lirb's 
or  Klumpke's  paralysis),  (454-5).     (Figs.  33,  38). 


Single  i 


nultiple  Neuromata,  (93S).    (Figs.  33,  38).     491 


Injury  or  inflammation  of  one  or  more  motor  cranial 
nerves  (facial  paralysis,  etc.),  (1301-7).    (Fig.  19.) 
Inflammation,  softening  or  hemorrhage  involving  one 
or  more  motor  cranial  nuclei  (motor  oculi  paraly- 
sis, etc.),  (1304).    (Figs.  18-21.) 
Lead  Palsy,  (584,  7S8,  1050). 

Acute  Anterior  Poliomyelitis.  Myelitis  of  the  An- 
terior Horns;  Infantile  Paralysis.  Acute  Atro- 
phic Paralysis.  Heine-Medin's  Disease,  (789, 
1148,  1233).    (Figs.  24-6.) 


Spinal  or  Neuritic  Muscular  Atrophy.  Peroneal 
type,  and Charcot-Marie-Tooth's  type,  of  muscular 
atrophy,  (696). 


Facio-scapulo-humeral  type, 
Landouzy-Dejerine  type, 
dystrophy,  (1152). 


Scapulo-humeral  type,  or  Erb's 
juvenile  form,  of  dystrophy 
(7S6,  1152).  J 

Pseudo-hypertrophic  Paralysis,  (780,  Hob) 


498 

Simple 

Idiopathic 

Muscular 

Dystrophy 


CHART  Xb 
Spastic  Paralysis 

Comprising  Numbers  178  to  481  on  left  side  of  Chart 
and  501  to  527  on  right  margin 


DIAGNOSTIC  SYMPTOMS  AND  TESTS 


473 

S 
P 
A 
S 
T 
I 
C 

P 
A 
R 
A 
L 
Y 
S 
I 

s 


47S 

Hemiplegia 

or  Diplegia  or 

Monoplegia 

(254-5,  258) 


479 

Hemiplegia,  or 

Monoplegia 

J..  I, "258) 

(See  also 

Syringomyelia — 

552,  837-9.) 


480 
Paraplegia 

C.V.7) 

(See  also 

Syringomyelia- 

552,  837-9.) 


481 
Paralysis  of  any  ex- 
tent :    local]  mono 
plegia,   hemiplegia, 
or  paraplegia 


Congenital  or  ac- 
quired in  infancy. 
There  may  be  fever 
or  apoplectic  symp- 
toms at  onset. 

Almost  always  in 
adults  and  after 
middle  life. 
Sudden  onset,  or 
stroke  (ictus),  usu- 
ally with  coma  (205 
and  1037),  or  with 
headache  or  vertigo 
and  mental  con- 
fusion. Not  infre- 
quently the  attack 
commences  with  a 
hemiplegia  which 
may  or  may  not 
be  followed  by 
coma. 


A  motor  paralysis  of  one  (infantile  hemiplegia)  or  both  sides  (Little's  dis 
are  common  and  may  mask  the  exaggerated  reflexes.  In  walking  then 
and  at  times  idiocy  or  insanity.  Frequently  there  is  a  partial  arrest  ol 
of  cerebral  diplegia,  bulbar  symptoms  (434)  are  present  without  fibrilli 
expressions,  etc., can  occur  involuntarily,  but  no  voluntary  motions.    T" 

Symptoms  of    irritation    (convulsions,    rigidity,  etc.)  are       The  disease  i 
more    pronounced  than   are    symptoms  of  paralysis.  ache  and   i 

Symptoms  of  paralysis  are  more  pronounced  than  those 
of  irritation  (convulsions  may  occur,  especially  in 
cortical  lesions  and  in  hemorrhage  into  the  ventricles, 
in  which  ease  lumbar  puncture  may  yield  a  bloody  fluid). 
The  paralysis  is  in  part  temporary  and  in  part  per- 
manent in  varying  degree.  Slow  improvement  with 
almost  perfect  recovery  in  rare  cases.  More  or  less 
permanent  mental  impairment,  often  very  slight. 
Usually  patients  are  more  emotional  than  previously. 
Exaggerated  reflexes  and  ankle-clonus  are  present  after 
coma  has  cleared  up.  Babinski  is  present  from  the 
start.  Puffing,  stertorous  respiration  is  common. 
Cheyne-Stokes  respiration  (435)  and  tracheal  rales  are 
very  unfavorable  symptoms. 


Gradual  onset  with- 
out coma,  except  as 
a  terminal  symp- 
tom. 


There  is  paralysis 
always  of  motion 
and  commonly  of 
sensation,  usually 
in  the  form  of  para- 
plegia, more  rarely 
in  the  form  of  a 
spinal  hemiplegia 
(442),  which  later 
may  become  a  para- 
plegia. The  re- 
flexes are  exagger- 
ated.  Ankle-clonus 
and  Babinski  are 
present .  Spasms 
and  contractures 
and  bed  sores  are 
often  present.  The 
organic  reflexes  are 
disordered.  The 
motor  paralysis  is 

permanent  or  lasts 
a  very  long  time. 
Sensory  paralysis 
may  be  slight  and 
transitory  and  may 
be  altogether  ab- 
sent. The  anesthe- 
sia is  often  limited 
above  by  a  narrow 
zone  of  hyperesl  he- 
sia. 


Paralysis  limited 
by  some  prominent 
anatomical  land- 
mark. 


Sensory  symptoms 
are  always  pres- 
ent. Organic  re- 
flexes are  normal 
or  only  slightly 
disordered. 


Brain  symptoms.  Steadily  in- 
creasing psychic  disorder,  and 
local  motor  and  sensory  disturb- 
ances over  the  same  area. 


A  sudden  att 

the  upper, 
balls,  awaj 

arterial  (lis 
face,  then 
hemiplegic 

Similar  to  th 
arterial  tei 
mon  than 

Similar  I"  t  li 
syphilis. 

k     basilar  art 

hemorrhag 
Headache,  v 

mon.  Clio 
more  rarel 
mental  du 
usually  pr< 
increased  t 
cempressio 


Spinal     symptoms.       Paralysis     of 

motion   and   sensation   on   oppo-       Characterise 

site  sides  of  body.  Symptoms 

spinal  epil 

The  paralysis  is  only  slight  and  follows  or  accomp 
a  paralysis  (chorea  mollis). 

Intention  tremor,  nystagmus,  scanning  speech,  ata 

r There  may  be  a  history  of  injury  and  a  fracture  ol 

No  history  of  injury.  Little  or  no  pain.  Sensor 
syphilitic  myelomalacia  (1211). 

May  be  history  of  remote  injury.  Much  pain  radia 
spinal  fluid. 

There  may  be  a  history  of  injury  and  a  fracture  o 

No  history  of  injury.     Little  or  no  pain.     Sensory  f 

tic  myelomalacia  (1211). 
May  be  a  history  of  remote  injury.    Much  girdle  pa 

Evidence  of  Pott's  disease  or  tumor  compressing  t 
pain.  In  cases  of  compression  due  to  Pott's  die 
uniler  increased  tension  and  may  contain  globul 

History  of  working  under  increased  atmospheric  pi 

Old  age,  atheromatous  arteries,  arterial  tension  usu 

Tumor  can  be  seen  or  felt  on  back  replacing  the 
is  involved,  or  not.    Club-foot  is  common, 

Signs  of  irritation  predominate  oyer  those  of    par 

unless  the  cord  is  also  involved.      Usually  a  hist 

Paralysis  purely  motor,  a  paresis  rat 

passive  motion,  especially  when   r: 

N"    'lav. a.  a  muiliple  Xerosis  (659).     Krb's  s; 

This  disease  may  be  simulated,  in 

There  is  a  combination  of  motor  pai 
IX|:|'  In  s e  cases,  especially  inward 

Tl  e  motor  paralysis  is    usually  accompanied  by    a   great  variety  of  sens  y 
the  physician  (imaginary  or  delusional  paralysis).     A  paralysed    limb 
retention  of  urine  is  common.     Hysterical  symptoms  (42.5).     Impossil 
this  is  sometimes  of  value  in  diagnosis. 


Choreic  symptoms. 

Cranial  and  spinal 
nerves  are  in- 
volved. 

Arms  and  legs  are 
paralysed.  Pri- 
apism is  com- 
mon, also  respira- 
tory difficulty 
and  early  death. 
Radiating  pains 
are  common. 


Legs  only  are  par- 
alysed. Girdle 
sensation         and 

pains      radiating 

into  the  extrem- 
ities are  common. 


Legs  mainly  in- 
volved. Arms 
involved  later 
and  slightly,  if  at 
all.  These  dis- 
eases may  occur 
in  severe  ane- 
mia. 


DIAGNOSTIC  ANALYSIS  OF  SYMPTOMS 

ABSTRACT  OF  SYMPTOMS 

the  body,  or  of  one  extremity,  without  anesthesia  and  with  very  little  muscular  atrophy  (from  disuse).  A  squint  is  common.  The  legs  are  often  mainly  or  alone  paralysed.  Rigidity  and  contractures 
l  adductor  spasm,  "scissors  gait"  (795-9).  Extensor  spasm  is  also  frequent.  Epileptiform  convulsions  are  common,  both  at  onset  and  during  the  course  of  the  disease.  There  is  much  mental  weakness 
of  the  paralysed  part.  Athetosis  and  post-hemiplegic  chorea  and  other  motor  disorders  are  common.  Speech  is  commonly  affected  (dysarthria).  The  organic  reflexes  are  not  disordered.  In  some  cases 
atrophy,  and  automatic  and  mimetic  actions  are  preserved.  In  such  cases  the  eyeballs  will  follow  a  light  or  other  object,  but  cannot  be  turned  by  any  effort  of  the  will,  and  laughing,  weeping,  emotional 
is  often  smaller  on  the  side  of  the  affected  cerebral  hemisphere. 

[he  result  of  injury.  When  not  so,  prodromal  symptoms  (432)  are  usually  present.  Convulsions  are  common,  both  at  the  onset  and  during  the  course  of  the  disease,  which  is  often  intermittent.  Head- 
npairment  are  frequent.     The  onset  of  paralysis  is  apoplectiform.     It  is  usually  motor  only,  is  rather  mild  in  degree  and  is  usually  transient.     Organic  reflexes  normal.     Cerebrospinal  fluid  often  bloody. 

laralysis  usually  of  one-half  of  the  body,  usually  of  motion  only,  rarely  of  sensation  only,  sometimes  of  both.    The  lower  branch  of  the  facial  nerve  is  much  more  completely  and  permanently  paralysed  than 
lay  lie  normal.     Onset  is  usually  accompanied  by  profound  coma  (205)  of  several  hours  or  days  duration,  but  not  always.     In  the    coma  there  is  oftenjurning  of  the  head,  and  conjugate  deviation  of  eye 
e  hemiplegic  side.     Pulse  is  slow.     Slight  variations  of  temperature  about  the  normal  point;  when  the  variation 
1  nephritis  and  usually  high  arterial  tension.     The  disease  usually 
leg  and    lastly  in  arm.     Contractures,  causing  flexion  of    joints  of    a: 
is1  urbances  occur  in  rare  cases. 


extreme  the  prognosis    is    bad.    Prodromata    are    rather    rare    (432).    There  is  often 
._  advanced  life.     If    death  does  not  occur  in  the  coma,  there  is  usually  more  or  less  improvement  in  the  paralysis;  first  in  the 
and  extension  of  joints  of  leg,  are  frequent  and  of  bad  prognosis  as  regards  recovery  from  the  paralysis.     Athetosis  and  other  post- 


but  onset  is  more  often  instantaneous  and  coma  is  usually  less  profound  and  long  and  frequently  is  entirely  absent.    There  are  no  prodromata.    There  is  cardiac  disease  or  other  source  for  an  embolus.    The 
jsually  low.     The  disease  usually  occurs  in  youth  or  middle  age.     In  general  the  symptoms  are  less  severe  and.  less  permanenMhan  in    hemorrhage.    Convulsions,  aphasia  and  monople;  -  - 
•rhage,  because  the  lesion  is  more  apt  to  be  cortical.     Multiple  (more  than  two)  recurrences  are  more  common  i 


i  embolism  than  in  hemorrhag 


but  onset  may  be  more  gradual,  although    still 
:rial  tension  is  usually  high.     Arterial  disease 
uore  frequently  affected.     Simultaneous  paralysis  of 
olism. 

smiting  and  convulsions,  general  or  local,  are  com- 
or  optic  neuritis  is  usually  present  in  tumor,  much 
cess.  Steadily  increasing  inertia  and  more  or  less 
Focal  symptoms,  both  spasmodic  and  paralytic,  are 
specially  Jacksonian  epilepsy  (431,605).  Markedly 
f  cerebro-spinal  fluid  and  slow  pulse  in  stage  of 
ially  in  tumor. 


sudden  and  even  at  times  instantaneous.  Prodromata  (432)  are  common.  Coma  is  more  frequently  absent  or  less  profound.  There  is  often  a  history  of 
is  common.  The  disease  usually  occurs  in  advanced  life.  Bulbar  symptoms  are  more  common  than  in  hemorrhage  or  embolism,  because  branches  of  the 
is  of  many  cortical  functions  is  more  common  than  in  hemorrhage.     Multiple  (more  than  two)  recurrences  are  more  common  in  thrombosis  than  in  either 

No  fever.    No  infection,  or  origin  for  abscess.    Chronic  course.    Steady  progression  of  all  symptoms.    Often  history  of    previous  remote  injury.    No  in- 
crease of  cellular  elements  found  in  the  blood  or  in  cerebro-spinal  fluid  obtained  by  lumbar  puncture.     Frequently  symptoms  irritative,  rather  tha 
paralytic.     Percussion  of  skull  over  region  of    tumor    often    shows    tenderness.    Headache    is    very  rarely  absent  and  is  usually  intense.     It  may  t 
local,  but  is  of  little  or  no  value  in  localizing  thetumor.    The  paralysis  commences  as  a  monoplegia  and  very  slowly  (weeks  or  months)extends, 


be 
or  months)exten< 

Often  fever.  A  source  of  infection,  especially  suppurative  diseases  of  the  ear.  Rapid  course,  except  that  a  latent  period  in  the  progress  is  common,  fol- 
lowed by  a  rapid  termination.  Delirium  is  common.  Often  a  history  of  a  recent  injury.  Leukocytosis  maybefound  in  thebloodand  in  thecerehro- 
spinal  fluid  obtained  by  puncture  (74).  Frequently  symptoms  rather  paralytic  than  irritative.  The  paralysis  commences  as  a  monoplegia  and  rather 
slowly  (days)  extends. 


3ms  are  motor  paralysis,  loss  of  muscle  sense  and  ataxia  on  one  side  of  the  body;  with  analgesia,  thermic  and  sometimes  tactile  anesthesia  of  other  side  (442).  Stationary,  or  steadily  progressive  chronic  course. 
ii"  bilateral  Reflexes  vary  with  the  position  of  the  tumor.  They  may  be  absent,  but  are  usually  increased  on  the  side  of  the  motor  paralysis,  and  are  so  greatly  increased  frequently  as  to  cause 
3). 


DIAGNOSIS 

Cerebral  Palsy  of  Childhood.  Porencephaly.  Acute 
encephalitis.  Infantile  hemiplegia  or  diplegia 
(Little's  disease).  (577,  (130,  70S,  104S,  10S6.) 
(Figs.  15-16.) 

Meningeal  Apoplexy.  Hemorrhage  in  cerebral 
meninges.  Pachymeningitis  Interna  Hemor- 
rhagica. Aneurism,  etc.  (5S8,  1060.)  (Figs. 
15-16.) 

Cerebral  Hemorrhage.  1 


504 

Cerebral 

Apoplexy. 

(432.  5SS,  832, 

856-7,      1043, 

1060-3.) 

(Figs.  15-7.) 

Cerebral  Thrombosis 
softening. 

Cerebral  Tumor,  including  Cyst. 

(536-42,  578,  587,  833.  849,  S55-61,    892,    908, 
960,  1047.)     (Figs.  15-17.) 


Cerebral  Abscess  or  localized  Meningitis. 

(578,  587,  907,  960,  965,  1045-6.)     (Figs.  15-17.) 


Spinal  Tumor  or  unilateral  spinal  lesion,  Rrown- 
Sequard's  paralvsis.  (442,  4Sli,  515,  519,  542,  551, 
826,  830-40,  975.  9.81,  1003.)     (Figs.  24-6.) 


506 
507 


attack  of  hemi-ehorea,  involving  the  same  side  of  the  body.     Sympto 


nay  be  bilateral,  but  are  then  difficult  of  recognition.     In    many  cases  the    hypotonia  (almost  invariably  present)    may  simulate      Choreic  Paralysis.     (622.) 


zularly  distributed  motor  and  sensory  paralysis. 

-ae  with  deformity.     The  knee-jerks  may  be  abolished  in  the  early  stages,  later  increased.     There  may  be  blood  in  the  cerebro-spinal  fluid. 


Much   pain    and  rigidity  and  spasm  of  back.     Symptoms  at  first  more  unilateral.    Local  pains.     May  be  i 


ased  tension  of  cerebri 


Very  acute  onset 
j  Acute  onset 
)  Chronic  onset 

Very  chronic  onset 


-ae  with  deformity.     The  knee-jerks  may  be  abolished  in  the  early  stages,  later  increased.     There  may  be  blood  in  the  cerebro-spinal  fluid.  Very  acute  onset 

is  and  disroders  of  the  organic  reflexes  are  almost  always  present.    A  history  or  other  evidence  of  syphilis  (1205)  is  often  present  in  cases  of  syphili-    )  Acute  onset 

)  Chronic  onset 


dity  and  spasm  in  back.    Symptoms  at  first   unilateral.    Local  pain.    The  tension  of  the  cerebro-spinal  fluid  may  be  increased. 


Very  chronic  onset 


Cervical  region  of  spinal 
cord  above  cervical  en- 
largement.    (Figs.  24-6.) 


Dorsal     region     of     spinal 
cord.     (Figs.  24-6.) 


lg..     Much  girdle  pain  and  radiating 
may  occur.      Cerebro-spinal  fluid  is      Compre 


.  Rigidity  and  spasms  in  muscles  of  legs  and  back  are  frequent.  Usually  intense  pain  when  spine  is  bent  or  moved  and  especially  on  getting  out  of  bed  in  the  mo: 
jre  may  be  no  sensory  symptoms.  Reflexes  may  be  so  exaggerated  as  to  constitute  spinal  epilepsy  (60-1,  443),  but  vary  according  to  seat  of  lesion.  Contractu 
ymphocytosis. 

Headache,  vertigo  and  vomiting  in  early  stage  of  disease. 

a,  loss  of  memory.    Emotional  and  exhibits  mental  impairment.     Paralysis  is  not  severe,  resembles  that  of  paralysis  agitans  without  tremor,  and  reflexes  of  all  kinds  are  not  much  altered. 

if  the  vertebrae,  or  the  cleft  can  be  felt  in  spine  without  any  visible  tumor  (occulta).     There  may  or  may  not   be  paralysis.     Reflexes  may  be  present  or  exaggerated  according  as  the  lumbar  enlargement 


earlv 


Paralysis  is  of  sudden  onset,  slight  in  degree  and  disappears  soon, 


Much  rigidity,  girdle  and  radiating  pains  and  spasm  in  back  muscles.     There  is  usually  spasmodic  retention  of  the  urine  ir 
injury.     Reflexes  exaggerated.     Lumbar  puncture  may  yield  a  bloody  fluid.     Symptoms  vary  with  position  of  hemorrhage, 
a  a  complete  paralysis,  very  slowly  progressive    and  often  stationary  during  long  periods.     Spasm,  rigidity  of  leg  muscles  and  later  contractures.    Greatly  exaggerated  reflexes.    Legs  offer  great  resistance  to 
Ankle-clonus,  Babinski  and  spinal  epilepsy  (443).    Organic  reflexes  little  if  at  all  disordered.    Arms  usually  not  affected,  but  may  be  slightly  so  after  years.     This  clinical  picture  is  at  limes  the  early  stage  oi 

spinal  paralysis, although  in  it  the  reflexes  are  not  always  greatly  exaggerated  and  the  posterior  columns  are  at  times  involved,  cannot  be  distinctly  separated  from  this  disease,  except  perhaps  by  its  etiology. 
nild  form,  with  exaggerated  knee  jerks,  but  without  ankle  clonus  or  Babinski,  and  with  marked  stiffness  of  legs,  as  the  result  of  reflex  action  from  irritation,  especially  from  the  genitals. 

ind  marked  ataxia  which    develop  very    gradually  and  slowly.     Some    moderate  pain  and  Tarely    there  may  be  anesthesia  and  analgesia.    The  tendon  reflexes  are  exaggerated.    Ankle-clonus  and  Babinski. 
d  of  the  disease  the  reflexes  may  be  abolished,  but  the  Babinski  persists.     It  is  a  disease  of  adult  life,  but  is  analogous  to  Friedreich's  ataxia  (652). 


:oms.  The  disease  is  usually  of  sudden  onset  and  often  follows  some  powerful  emotion.  It  is  usually  permanent  until  cured  by  another  strong  emotion,  which  may  be  ofte: 
rs  great  resistance  to  passive  motion,  even  to  slow  motion.  Contractures  are  common.  Knee-jerks  are  usually  increased,  but  no  true  ankle-clonus  or  Babinski.  Organic  rette> 
^plaining  all  of  the  symptoms  by  any  one  organic  lesion.     The  paralysis  is  not  limited  to  one  muscle,  or  to  the  distribution  of 


nerve.     Associate.  1  movements  do  not  occur  i 


artificially  produced  by 
is  rarely  disturbed,  but 
hysterical  paralysis,  and 


Disseminated  Sclerosis.      (580,  659,  668, 

688,  756,  765,  799,  913,  1051.) 
Injury  or  hemorrhage  in, 

Acute  myelitis  or  myelomalacia  of,     (795,  S2S.) 
Chronic  myelitis  or  myelomalacia  of, 
Tumor  in, 

Injury  or  hemorrhage  in, 

Acute  myelitis  or  myelomalacia  of,     (795,  S29.) 
Chronic  myelitis  or  myelomalacia  of, 
Tumor  in, 


l  Myelitis.    (795.)    (Fig.  27.) 


Caisson  disease  or  Diver's  paralysis. 
Senile  Paraplegia.     (791a) 
Spina-bifida. 

Hemorrhage  in  spinal  membranes.  Hemator- 
rhachis.     (973.) 

Spastic  Paraplegia  or  lateral  sclerosis  (usually 
symptomatic  and  part  of  a  more  extensive 
lesion,  spinal  or  cerebral.)     (797.)     (Figs.  24-7.) 

Ataxic  Paraplegia  or  postero-lateral  sclerosis. 
(660,  796.)     (Figs.  24-6.) 

Hysterical  Paralysis. 

(747-8,  759,  793,  878,  1074.) 


512 
513 
514 
515 


CHART  Xc 

Combined  and  Intermittent  Paralysis 

Comprising  Numbers  171  and  174  on  left  side  of  Chart 
and  ">:r>  to  656  on  right  margin 


131 


DIAGNOSTIC  SYMPTOMS  AND  TESTS 


474 
C 
O 
M 
B 
I 

N 
E 
D 

P 
A 
R 
A 
L 
Y 

I 

S 


Cranial   and   spinal 
nerves  involved. 
(Figs.  1S-23, 33, 38.) 


Sensory  symptoms 
present  usually. 


'Bilateral  symp- 
toms. 


Crossed  paralysis 
(256)    and    bulbar 
symptoms  (434). 


Spinal  nerves  alone 

involved. 

(Figs.  24-7,  33,  38.) 


No  sensoiy 
symptoms. 


No  sensory 
symptoms. 


If  1 1  io  patient  does  not  promptly  die,  one  or  mot 
gia  (525).  There  arc  usually  dysarthria,  dysp] 
toms  at  first  may  lie  more  unilateral. 


Paralysis  of  one  or  more  eye  muscles  of  one  side 


Paralysis  of  facial  (both  upper  and  lower  branch- 


Paralysis  of  hypoglossus  of  one  side  and  of  arm 


The  onset  of  paralysis  is  sudden.  If  the  patient 
sive.  They  are  usually  unilateral,  but  may  Ik 
paralysed,  while  there  is  a  spastic  paralysis  in 
.May  he  duo  to  acute  inflammation,  hemorrhai 
myelitis.    Often  due  to  syphilitic  endarteritis  i 


Chronic — The  chronic  forms  of  these 
diseases,  with  the  spinal  form  (547), 
constitute  the  progressive  muscular 
atrophies  and  resemble  the  muscular 
dystrophies  in  that  the  paralysis  and 
atrophy  advance  together  slowly,  and 
it  is  difficult  to  say  which  is  primary. 
They  also  constitute  a  group  of  chronic 
degenerative  atrophies.  n 

Symmetrical  para!-      The  muscles  affected  show  progressive  weakness, 
ysis  commencing  in  or,  more  rarely,  in  the  muscles  of  the  shoulder 

the  small  muscles  of  thumb  cannot  be  brought   across  hand  to  tone 

hands  or  in  shoul-  but  not  always.    There  are  secondary  contract 

dex  girdle  muscles.  of  muscles  is  increased.     Often   associated 

umns  are  involved  or  not.     It  is  difficult  to  di 


'  The  paralysis  in- 
volves I  lie  eye  mus- 
cles. 

The    paralysis     in- 
volves    the     lips, 
tongue,       pharynx 
I  and  larynx. 


P 

Th< 


Marked  sensory 
symptoms  are  pres- 
ent, such  as  pain, 
paresthesiae,  anes- 
thesia, etc.,  with 
the    motor   paraly- 


Dissociation  of  sen- 
sation (3C5)  is  pres- 
ent. 


r 


ery  acute  onset .    Sympti 

may  yield  a  bloody  fiuii 


Acute,  sub-acute  or  chroni 
litic  m\ elomalacia  i,l-l  1 

Chronic  course,  intense  pa 
common.    Cerebro-spina 

Very  chronic  onset  and  a 


All  the  muscles  of 
the  body  and  head. 


Muscles  of  one  or 
both  legs,  rarely  of 


Commencing  in  legs 
extending  to  arms. 


Associated   with    a 
cervical  rib 


Both  arms  and  legs  are  paralysed.  There 
are  trophic  disturbances  in  the  arms 
and  not  in  the  legs.  Pupils  are  often 
unequal.  Reflexes  are  abolished  in  the 
arms  and  increased  in  the  legs.  Bab- 
inski  and  ankle-clonus  are  present.  The 
bladder  is  usually  more  or  less  dis- 
tended; its  detrusor  being  paralysed. 
Contractures  may  be  present  in  tin'  legs. 

Dissociation  of  sensation  is  the  most  characteristic  symptom  and  is  co 
Trophic  lesions  are  usually  prominent.  Pemphigus,  ulceration  and 
trophic  symptoms  predominate  over  motor  symptoms  in  the  arms; 
present  the  symptoms  may  be  both  in  arms  and  legs,  and  the  mote 
aggerated  in  central  gliosis  in  the  cervical  or  dorsal  regions.  The  cer 
fairly  rapid  course,  and  may  exhibit  a  unilateral,  spastic,  muscular  ] 

The  characteristic  sign  of  the  disease  is  the  rapid  tiring  of  the  muscles  when  in  activity.  P»1 
(401).  There  is  no  muscular  atrophy  and  no  reaction  of  degeneration.  In  the  domain  ol  i 
usually  held  retracted  on  account  of  the  ptosis.    The  symptoms  are  slight  in  the  morning 

Intermittent  attacks  of  painful  muscle  cramp,  and  weakness  of  leg  or  legs,  caused  by  walkinf 
Rarely  the  disease  occurs  in  one  or  both  arms.  No  sensory  disturbances  except  painful  crai 

Recurrent  attacks  of  paralysis  of  the  muscles  of  the  legs  usually  first  and  then  of  arms,  las 
nerves  are  not  attacked.  There  is  usually  well  marked  heredity,  or  the  disease  occurs  in  1 
but  in  some  groups  of  family  periodic  paralysis  these  negative  symptoms  are  not  present. 

A  cervical  rib  can  be  felt  and  can  be  seen  with  the  X-ray.  In  some  cases  of  cervical  rib,  att; 
skin  which  comes  on  after  the  arm  has  been  used  a  short  time,  and,  if  use  of  the  arm  is  co 
be  Caused  by  a  cervical  rib,  and  then  is  often  relief  by  elevation  of  the  arm  and  is  made  V 


DIAGNOSTIC  ANALYSIS  OF  SYMPTOMS 
ABSTRACT  OF  SYMPTOMS 


No  optic  neuritis.    A  variety  of  apoplexy  (504).    No  increased  tension  of  cerebro-spinal  fluid. 


al  nerves  are  paralysed.     There  is  more  or  less  marked  spastic  paraple-   f  Acute  onset.    Regressive  c 
taxia,  anesthesia  and  often  vertigo.    (Bulbar  symptoms— 434.)    Symp-  \ 

[  Chronic  onset.     Progressive  course.     Optic  neuritis.     May  be  increased  tension  of  cerebro-spinal  fluid. 


arm  and  leg  of  opposite  side. 

igeminal  nerve  on  one  side  and  of  arm  and  leg  of  opposite  side. 

;  of  opposite  side. 


{Acute  onset  and  regressive  course.     No  optic  neuritis.     No  increased  tension  of  cerebro-spinal  fluid. 
Chronic  onset  and  progressive  course  and  optic  neuritis.     May  be  increased  tension  of  cerebro-spinal  fluid. 
f  Acute  onset  and  regressive  course.     No  optic  neuritis.     No  increased  tension  of  cerebro-spinal  fluid. 
[  Chronic  onset  and  progressive  course  and  optic  neuritis.     May  be  increased  tension  of  cerebro-spinal  fluid. 

{Acute  onset  and  regressive  course.     No  optic  neuritis.     No  increased  tension  of  cerebro-spinal  fluid. 
Chronic  onset  and  progressive  course  and  optic  neuritis.     May  be  increased  tension  of  cerebro-spinal  fluid. 

;  so  that  ptos: 


There  is  more  or  less  extensive  paralysis  of  the  motor  nerves  of  eyeball  (3rd,  4th  and  t 
vision,  nystagmus,  etc.,  may  result. 


3t  die  promptly,  later  the  symptoms  are  regressive  rather  than  progres- 

:al.    A  number  of  cranial  nerves,  either  motor  or  sensory,  or  both,  are 

ess  pronounced  in  the  arms  and  legs.     Vertigo  is  a  common  symptom.  ^ 

■mhosis,  embolism,  or  compression.     May  occur  in  acute  anterior  polio-    I  There  is  paralysis  of  the  lips,  tongue,  pharynx  and  larynx  (7th,  9th,  10th,  11th  and  12th  nerves),  with  consequent  dysar- 

litic  neuritis.  L      thria  and  dysphagia  and  usually  ataxia  and  respiratory  disturbances. 

onset,  of  weakness  of  ocular  muscles.  It  may  be  steadily  progressive  or,  having  progressed  to  a  certain  point,  it  may  remain  stationary.  Muscles  may  be  attacked  in  any  order,  ptosis,  squint,  im- 
yeballs,  immobile  pupils.  The  disease  may  attack  only  the  external  muscles  of  the  eyeball  (ophthalmoplegia  externa),  or  only  the  internal  muscles  (ophthalmoplegia  interna),  or  both,  (ophthalmo- 
impleta).    Disease  may  be  complicated  by  bulbar  paralysis  (54G)  and  is  usually  associated  with  amyotrophic  lateral  sclerosis. 

s  bent  forward.  There  are  bulbar  symptoms  (434).  There  are  drooling  of  saliva,  dysarthria,  dysphagia,  and  aphonia.  Paralysis,  tremor,  atrophy,  fibrillary  contraction  of  muscle  of  tongue,  lips, 
harynx,  larynx,  etc.  Both  facial  nerves  are  involved  in  some  cases.  The  paralysis  very  slowly  progresses.  There  are  symptoms  of  a  mild  spastic  paraplegia  in  legs  with  ankle-clonus  and  Babinski. 
e  of  advanced  life.  Often  associated  with  amyotrophic  lateral  sclerosis  and  at  times  with  progressive  ophthalmoplegia  (545).  In  addition  to  the  pseudo-bulbar  paralysis  of  myasthenia  gravis  (553) 
another  form  due  to  lesions  in  both  cerebral  hemispheres  in  which  there  is  no  muscle  atrophy,  or  fibrillation,  and  no  change  in  the  electrical  reaction,  but  all  the  other  symptoms  of  bulbar  paralysis 
less  marked.    There  is  more  mental  impairment  and  greater   emotional  excitability  than    in  true  bulbar  paralysis. 

y,  fibrillary  contractions  and  all  degrees  of  alteration  in  electrical  excitability  from  simple  diminution  to  complete  reaction  of  degeneration.  The  process  commences  in  the  small  muscles  of  the  hands, 
scapulo-humeral  type),  is  usually  fairly  symmetrical  and  extends  to  the  other  groups  of  muscles  in  arms,  body  and  even  legs.  The  muscular  weakness  follows  and  is  dependent  upon  the  atrophy.  The 
ittle  finger  The  fingers  cannot  be  spread  apart,  nor  can  their  last  two  phalanges  be  extended  on  the  first.  The  legs  show  a  mild  degree  of  spastic  paraplegia,  with  ankle-clonus  and  often  Babinski, 
specially  the"  claw  hand."  The  head  is  usually  bent  forward  and  there  is  much  deformity  about  shoulder  and  other  parts.  A  disease  of  adult  life,  and  of  very  chronic  course.  Mechanical  irritability 
agressive  bulbar  paralysis  (54G).  Some  authors  divide  this  symptom  complex  into  two  groups  according  as  to  whether  the  atrophy  or  the  paralysis  is  primary,  and  as  to  whether  the  lateral  col- 
i  such  distinction  clinically,     The  one  form  may  be  an  earlier  stage  of  the  other. 


most  extensive  in  first  few  days  and  may  slowly  improve  later.    May  be  deformity  in  cervical  region  of  spine.     Knee-jerks  may  be  absent  in  early  sto 


Lumbar  punetu 


Symptoms  continue  to  extend  for  t 


Cervical 

ment  of  spinal  cord. 

(Figs.  24-6.) 


:  time  and  are  fairly  symmetrical.    Organic  reflexes  disordered.     A  history  or  other  evidence  of  syphilis  (1205)  is  often  foundin  syphi- 

and  neck  precede  the  paralysis  and  contractures  and  muscular  atrophy  in  hands,  "  claw  hand."      Cutaneous  eruptions  (herpes,  pemphigus,  etc.)  are  not  un- 
may  be  under  increased  tension  and  show  lymphocytosis.     Most  of  these  cases  are  the  result  of  chronic  syphilitic  meningitis. 

ssive  course.     Symptoms  at  first  mainly  unilateral,  becoming  bilateral  later.     Cerebro-spinal  fluid  may  show  increased  tension. 

with  pain  and  paresthesiae  and  more  or  less  motor  paralysis  and  atrophy.     The  muscular  atrophy  has  often  the  location  and  characteristics  of  that  of  progressive  spinal  muscular  atrophy  (547). 

ion  of  the  hands  and  trophic  lesions  of  bones,  muscles,  and  other  tissues  occur  in  the  type  called  Morvan's  disease.  In  the  most  common  form  the  cervical  region  is  alone  affected  and  sensory  and 
he  legs  show  a  mild  spastic  paraplegia  (525),  and  scoliosis  or  kyphosis  occur  in  more  than  half  the  cases.  Paradoxical  (379)  and  spontaneous  sensations  have  been  noted.  When  a  diffuse  glioma  is 
itoms  are  about  as  prominent  as  the  sensory  and  may  be  unilateral  in  the  early  stages..  All  forms  of  reflex  action  are  abolished  when  the  cervical  and  lumbar  enlargements  are  involved,  but  are  ex- 
>rm  of  the  disease  runs  a  chronic  course,  extending  at  times  over  decades,  but  slowly  progresses  and  the  anesthesia  at  first  slight  steadily  becomes  more  marked.  The  diffuse  form  often  runs  a 
s,  at  least  in  the  early  stages. 

i  walk  well  at  the  start,  but  after  a  few  (or  a  few  hundred)  steps  is  tired  out.  The  same  is  true  of  all  other  voluntary  acts.  Examination  of  the  muscles  with  electricity  gives  the  myasthenic  reaction 
nerves  (in  which  the  case  usually  commences)  there  may  be  ptosis,  diplopia,  ophthalmoplegia,  diplegia  facialis,  dysarthria,  dysmasesia,  etc.,  and  all  the  spinal  nerves  may  be  affected.  The  head  is 
jw  worse  during  the  day.    No  sensory  disturbances  except  painful  cramps.    Organic  reflexes  normal. 

ng  the  attack  the  feet  are  cold,  and  there  is  diminished  or  absent  pulsation  in  arteries  of  feet,  associated  with  marked  arterio-sclerosis  of  arteries  of  leg  as  shown  by  palpation  and  by  the  X-ray. 
rganic  reflexes  normal.  Angio-spastic  hemiplegia  in  which  temporary  attacks  of  hemiplegia,  sometimes  associated  with  aphasia,  occur,  is  probably  a  variety  of  this  disease. 

few  hours  or  days.  The  attacks  usually  occur  in  the  morning  or  after  rest.  During  the  attack  the  left  cardiac  ventricle  may  become  temporarily  dilated  and  a  murmur  may  be  heard.  The  cranial 
groups.  During  a  severe  attack  there  is  often  a  diminution  or  absence  of' the  reflexes  and  of  the  faradie  and  galvanic  excitability  of  the  nerves,  and  of  the  mechanical  excitability  of  the  muscles, 
of  these  cases  are  apparently  due  to  malaria  and  can  be  cured  by  the  administration  of  quinine. 

:cur,  but  only  after  use  of  the  arm.  These  attacks  are  usually  unilateral,  even  though  the  extra  rib  is  on  both  sides.  The  attack  consists  of  numbness,  tingling,  feeling  of  congestion,  redness  of  the 
d,the  arm  shows  a  decided  paresis,  which  passes  off  if  the  arm  is  kept  at  rest.  An  ununited  fracture  of  the  clavicle  will  rarely  cause  similar  symptoms.  Pain,  in  the  form  of  a  brachial  neuralgia,  may 
>y  motion.     In  rare  cases  this  paralysis,  at  first  intermittent,  may  become  permanent  and    may  be  associated  with  atrophy  of  the  muscles  of  the  hand  and  even  of  the  forearm. 


Hemorrhage,  softening  or  acute  inflammation  in  brain-stem     535 

(543-4,  656). 
Tumor  in,  or  compressing  the  brain-stem  (656).  536 

Hemorrhage  or  softening  in  crus  cerebri  (543).  537 

Tumor  in,  or  compressing  'crus  cerebri  (656).  538 

Hemorrhage  or  softening  in  pons  (543).  539 

Tumor  in,  or  compressing  pons  (656).  540 

Hemorrhage  or  softening  in  medulla  (544).  541 

Tumor  in,  or  compressing  medulla  (656).  542 

Acute  or  Apoplectiform  Polioencephalitis  Superior  (495,  535,     543 
1064). 

Acute  or  Apoplectiform  Polioencephalitis  Inferior.  Acute  Bui-     544 
bar  paralysis  (495,  535,  1064). 

Progressive   Ophthalmoplegia.  Polioencephalitis  Superior    545 

Chronica  (often   symptomatic   of   a   steadily   progressive, 
more  widespread  disease,  such  as  tabes,  tumor,  etc.). 

Progressive    Bulbar     Paralysis.       Polioencephalitis     Inferior    546 
Chronica.       Labio-glosso-pharyngeal  Paralysis,    (G94.    761, 
1150). 


Amyotrophic  Lateral  Sclerosis.     Progressive  Spinal  Muscular    547 
Atrophy.  Aran-Duchenne  type  of  muscular  atrophy.  Chronic 
Atrophic  Paralysis,  (095,  797,  1149). 


'  Injury  of,  or  hemorrhage  in,  548 

Acute  or  chronic  myelitis  or  myelomalacia  of,  (795, 835, 1310).  549 

Pachymeningitis  hypertrophica  cervicalis.  550 

.Tumor  in,  or  compressing,  (836)  551 

Syringomyelia.     Central    gliosis.      Morvan's    Disease,    (693,  552 
837-9,  1009,  1150a,  1170,  11S7,  1357,  1359). 


Myasthenia  gravis.    Pseudo-bulbar  Paralysis. 


Intermittent     Limping    or    Claudication.    Dysbasia    Angio-     554 
sclerotica,  (1199). 


Family  Periodic  Paralysis. 

Pressure  of  cervical  rib  upon  sub-clavian  artery. 


CHART  XI 

Convulsion  or  Spasm 


DIAGNOSTIC  ANALYSIS  OF  SYMPTOMS 
Tests 


SYMPTOM 

Analyzed 

Character 

Extent 

.571 

CLONIC 
mainly  (246) 

'     GENERAL 
CONVULSION 

LOCAL               i 
CLONIC 
.SPASM 

570 
CONVULSION 

OB   SI 'ASM 

(242) 

572 

TONIC 

mainly  (245)     * 

'general 

TONIC 
SPASM 

LOCAL 

TONIC 
.SPASM               J 

573 
CHOREIFORM 

(272) 

- 
574 

Diseases  in  wbio 

arc  sit  forth  in 

VHIITOID 
I      (271) 

Diseases  in  which   convulsions  occur 
set  forth  in  Chart  XI  a. 


Diseases  in  which  local  clonic  and  all 
forms  of  tonic  spasm  occur  are  set 
forth  in  Chart  XI  b. 


188 


CHART  XI  a 

General  Clonic  Convulsion 


( !omprising  Numbers  571  on  left  side  of  Chart 
and  575  to  596  on  right  margin 


L35 


DIAGNOSTIC  SYMPTOMS  AND  TES1  S 


(-Repeated  attacks. 


The  convulsion 
commences  in  all 
the  muscles  at 
about  the  same 
time  (epileptiform 
convulsion). 


671 

G 
E 
N 
E 
R 
A 
L 

C 
L 
O 

N 
I 
C 

C 

o 

N 
V 

u 

L 

s 
I 
o 

N 


Apyrexia. 


Loss  of  conscious- 
ness, (coma  or 
semi-coma)  (205). 
Frequently  biting 
of  the  tongue  or 
other  injury.  Short 
duration. 


No  other  symptom 
of  disease  except 
the  convulsion. 


Symptoms  of  seri- 
ous brain  disease. 


One  attack  or  one 
^series  of  attacks. 


Congenital     or     in 
infancy.  Often 

fever    at    onset    of 
first  convulsion. 

In  youth   or  more 
.often  in  adults. 


Symptoms  of  cerebro-spinal  disease. 

f  Kidney  disease. 
Symptoms    of    dis- 
^Sl°L°}]ielZTgaDS  j  Cardiac  disease. 

(.Blood  disease. 


than  the  brain 


followe 

I  i. hi  of 

tile,  au 

tendon 

spots  a 

pressur 

spasm 

around 

attack 

Such  p 

observ; 

A  con  villi 
and  nc 
periphe 

The  disea 
rarely 

are  ran 

Between 
are  foil 
of  the 
sympti 
disease 
psychic 
vance  1 

Intent  ior 

There  an 

and  th 

Slow  pul: 

Rapid  fc 
culatio 


o         .  _        ,        •      (  Blue  line  on  gums,  lead  in  urint 
Symptoms   of  poi-    )  b        ' 

soninS-  I  Alcoholic  odor  of  breath  and  g( 


Apparent,  but  no  true,  coma  (shown  In- 
susceptibility to  suggestion).  No  biting 
of  tongue  or  other  injury.  Long  dura- 
tion. 


Symptoms   of   hys-  The  attai 

teria   1 125).     Such  very  ii 

attacks  have  been  usually 

called    hystero-epi-  orbital 

lepsy.  tomfl  | 


The  convulsion  always  commences  in  one 
group  of  muscles  and  later  extends 
over  the  whole  or  part  of  one  side  of 
the  body  and  often  over  both  sides. 

Jacksonian  epilepsy  (431). 


■s  Hyperpyrexia.      Epileptiform  convulsion. 


If  the  convulsion  remains  unilateral,  con- 
sciousness may  or  may  not  be  lost, 
usually  not,  but  it  is  always  lost  when 
the  convulsion  becomes  bilateral. 


Coma  during  and  after  the  convulsion. 


There    a 
present 
of  scriou: 
ease, 
always. 


Occurs  s 


Pyrexia. 

See  also  577. 


Lumbar  puncture  gives  a  clear 
bloody  or  purulent,  fluid,  unde 
pressure  containing  globulin 
polymorphonuclear  leucocyte.' 

Lumbar  punct  ure  gives  a  clear  f 
increased  tension  and  contaii 
ulin   and   many   mononucleai 
cytes,    and    if    the    disease 
polymorphonuclear  leucocytes 

Lumbar  puncture  gives  a  clear  f 
increased  tension,  but  no  ii 
cellular  elements. 

.     .  .        (  May  occur  in  children  at  the  onset  of  any  infectious  disease,  especially  in  < 

•convulsion.  |  js  tng  resuit  of  some  unusUal  metabolic  changes  within  the  body,  and  espe 


'Epileptiform    con- 
convulsion. 
Comat  during    and 
usually    after    the 
convulsion. 


Headache,  backache  and  radiating  pains, 
delirium,  vertigo  and  vomiting,  espe- 
cially on  change  of  posture,  hyperalge- 
sia (spinal  and  elsewhere),  photophobia, 
etc.,  are  early  symptoms.  Retraction 
of  head,  opisthotonus,  etc.  (265).  Pa- 
ralysis of  cranial  nerves  (squint,  etc.), 
cutaneous  eruptions  (herpes),  t&ches 
cer<5brales  and  Kernig's  symptom  (319). 
Tonic  spasm  and  paralysis  are  more 
common  in  basic  inflammations,  and 
clonic  spasm  in  cortical  inflammations. 


DIAGNOSTIC  ANALYSIS  OF  SYMPTOMS 


ABSTRACT  OF  SYMPTOMS 

:  with  arrest  of  respiration.    The  face,  at  first  pale,  soon  .becomes  pushed  and^cyanoth 


.*,.    The  pupil  is  dilated  and  inactive.     This  tonic  state  is  quickly 
the  major  attack  (le  grand  mal),  is  at  first    onic  with  arrest  of  respiration      The  face  at  first  pale ;  soon ™    ™-    ,     tongue, which  isoften  bitten  during  the  attack.    There  is  often  lateral  devia- 
,  minute)  by  clonic  spasm  of  longer  duration  (i  to  5  minutes)  with  noisy  respiration    and  irotl   on  1  ps  o Iten  mo     J  twi,chir|  of  certain  muScles,  "  motor  aura,"  or  by  a  sensory  hallucination  (tac- 

and  eyeballs  and  nystagmus     At  t.mes  urine  and  feces  are  passed  during    he  attack.    The  attack  s  °f ' en  preceuea    J  »  temperature  of  the  body  is  raised  and  albuminuria  is  frequent.    The 

risual,  olfactory,  etc.)  called  the  "sensory  aura"  (430)  and  is  often  usheied  '"  ^ a  "^ '      *'ie  «P''f P'l0,^/^^"    weakness  (stage  of  exhaustion)  often  follow  the  attack.    After  a  violent  atlack  purpuric 
are  occasionally  absent  during  and  immediately  after  the  attack.    A  deep  sleep  an 1  some  ™*cular^  at  varving  in.ervals,  but  attacks  can  neither  be  brought  on  nor  arrested  by 

nf'LTthe  ^^^J^-^^-^^^-^^^-^^^  lV"oCi,;Jl  enllensv)?   The  attacks  vary  Jreatly  in  character.    A1  times  there  is  merely  rigidity  without  clonic 
media).    At  times  there  '-  ~ 


ace     Complete  amnesia  in  regard  to  it  always  follow  an  attack.     There  are  recurrences  at  varying  intervals    oui.  jiuu    c, 

»  ihMta%"^y  a^ghtor  while  asleep  by  day  (nocturnal  epilepsy; .The attacks ;  vary -greasy  ,r ^a™te,    A     , 

»  media).    At  times  tliere  is  merely  loss  of  consciousness  without  action  or  with  some  automatic  art:    he minor  at  ack     e  pe Mmal^  At a.mesjhe  patient  is 

^cS^re^^ 


unconscious  and  runs  forwards  ana  turns 

an  act  of  violence  (epileptic  mania).     At  times  an 

more  or  less  mental  impairment  (epileptic  dementia). 

The  diagnosis  of  malingering  can  only  be  made  by  long 


m  in  syphilitic  and  rachitic  children,  but  occurring  also  in  adults   especially  in  P«g--y   altogether  similar  (epileptiform)  to  the  above   but  occ urring  only  °nce   or 


ck,  especially  common 

ed.     Associated  often  w,,..  .... 

ition  and  at  the  onset  of  an  acute  infection.     No  sharp  line  can  be  drawn  between  these  convulsic 

.      h.mit)leeia  or  diplegia,  with  cons  derable  mental  impairment.      There  is  usually  dysarthria, 

genital  or  begins  in  early  infancy     Umlatera   or  b.'atera     convu  sions   occur ^^J^^fZre  orTs  complete  a?re!t  of  development,  physical  and  mental.     The  shape  and  size  of  the  skull 
often  post-hemiplegic  motor  disturbances:  athetosis,  rigidity  anrl  contractures,     i  requemiy  lueie  is,  «■•«  "  r 

xl.     Cases  of  epileptic  idiocy  may  belong  to  this  class,  even  though  they  present  no  paralysis. 

Headache,  vertigo  and  vomiting.     Choked  disc  or  optic  neuritis.     More  or   less  motor  ™d  sensory  paralys. 
loss  of  memory.     Localizing  symptoms  are  sometimes  present.     Convulsions  are  often  local. 

,.     ■„  .i  j  i     •         r,    „„ll„  „f  wiiaiinnl  and  ™mntoms  of  insanity.     Poor   judgment.    Good  natured  but  irascible.    Childish.    Characteristic  blurred 

Loss  of  will  power,  restlessness,  delusions  ^^Jf^^^PX^^'^^  and  apraxia).     Unequal  and  irregular  pupils,  Argyll-Robertson's  pupil,  optic  neu- 
speech.    Tremor  of  lower  facial  muscles,  lips,  tongue  and  hands,  and  aokoaraness  (aiaxu  j™^  ^    ^   J  ,  .,._   i.  t   .  ,,._;,,..,;  u-.  J,.,-!,,-,,,,,  ve:,ctii,n  i41fl-20i. 
ritis  or  atrophy.  L  History  of  syphilis.     Lumbar  puncture  shows  lymphocyto 


vulsive  attacks,  which 
■  a  temporary  weakness 
s  involved,  there  are 
steadily  progressing  brain 
rally  motor,  sensory  and 
Dms,  and  a  steady  ad- 
;oma  or  dementia. 


more  or  less  complete  arrest  of  development,  physit 

Mental  inertia  (apathy)  and  increasing  mental  weakness  and 


cerebrospinal  fluid,  globulin  and  a  positive  Wassermann  reaction  (419-20). 


,  scanning  speech,  nystagmus,  unsteady  gait,  motor  and  sensory  paralyses,  many  symptoms  of  Ideal  lesion,  etc. 

g  intermission  in  heart  beats  associated  with  coma  and  convulsions,  which  pass  off  after  the  heart  begins  beating  again.    Arteries  atheromatous.    Advanced  life 

;e  of  small  volume.    Insufficient  amount  of  blood  or  of  red  cells  and  hemoglobin.    Pallor,  dyspnoea 
esent.    Often  the  result  of  one  large  or  of  repeated  hemorrhages. 

aking  K.I.    Wrist-drop.    History  of  lead  colic  and  of  exposure  to  lead. 

emor  and  nervousness.    Muscular  tenderness.    History  of  alcoholic  abuse. 


DIAGNOSIS 

Idiopathic  Epilepsy  (including  the  major  attack,  the 
minor  attack,  epilepsia  media,  nocturnal  epilepsy, 
epileptic  automatism,  epileptic  mania,  psychic 
equivalent,  epileptic  dementia),  (110,  126,  430, 
846,  1027,  1058,  1071,  10S3,  1102). 


Eclampsia,  (1059). 


Cerebral  Palsy  of  Childhood.     Porencephaly.  577 

(501,  630,  798,  104S,  10S6). 

Cerebral  Tumor  (including  abscess  and  cyst)  not  in     578 
or  near  motor  area  of  cortex  (507-8,  587). 

Paresis.      General    Paresis.      Paralytic    Dementia,     579 
(134,  177,  416,  419-20,  675,  763,  895,  1049,  1104, 
1216,  1230). 

Disseminated  Sclerosis,  580 

(511,   659,   668,   68S,   756,  765,  799,  913,  1051). 


usually  high,  the    heart  hypertrophied,       Uremic  convulsion,  (576,  S50,  956). 


usually, 
exertion  and  strabismus  are  common.    Often  severe  digestive  disorders  with  congested  portal  i 


■ays  in  the  presence  of  an  audience.  There  is  always  a  warning  in  the  form  of  globus  hystericr, 
and  violent  and  many  of  the  movements  seem  purposeful  and  to  be  theatrical  posing  crucin 
long  time,  especially  if  the  audience  be  excited.  Eyes  are  usually  closed  and  the  eyeballs  tun 
etc.,  especially  if  the  audience  be  sent  from  the  room.  Moderate  pressure  upon  these  parts 
Vbundant  limpid  urine  after  the  attack,  but  urine  and  feces 


The  convulsion  often  commences  with  a  motor  (twitching),  rarely  with  a  sensory  (tingling), 
aura.  It  spreads  first  through  the  whole  of  the  part  first  attacked  and  then  in  a  definite 
order  from  face  to  arm,  or  from  arm  to  leg  or  face,  or  from  leg  to  arm  according  to  the 
anatomical  arrangement  of  the  cortical  motor  centers;  hence  never  from  leg  to  face  without 
the  arm  being  involved.  The  convulsion  is  followed  bya  hemiplegia,  sometimes  transient, 
sometimes  permanent  and  progressive.  There  may  be  muscular  rigidity  in  the  intervals 
between  the  convulsive  attacks. 


mlnitation    etc      Patient  may  fall  or  glide  to  the  ground  but  does  not  hurt,  herself.    The  convulsion  is 
'on     et!    and  assumed  attitudes,  (attitudes  passioneltes).     Patients  often  "rave"  during  the  attack,  which 
upwards  if  eyelids  are  forced  open.    Attack  can  usually  be  arrested  by  pressure  on  ovarian  region,  supra- 
lay  cause  an  attack.  Great  variety  of  sensory  symptoms, 
never  passed  Involuntarily  during  an  attack.    The  reflexes 

Occurs  in  youth  or  middle  age  and  often  after  traumatism  of  old  date.    Headache, 
ing.    Usually  choked  disc  or  optic  neuritis.    Symptoms  sum, lily  progressive. 
out  choked  disc  may  occur  in  localized  meningitis  or  other  irritative  lesions  lr 

Occurs  in  old  age  and  often  after  recent  injury.  Alcoholism,  atheromatous  arteries  and  insanity  are 
common  Sudden  apoplectic  attack  with  improvement  later.  No  choked  disc.  Symptoms  pro- 
gress paroxysmally,  and  after  each  paroxysm  there  is  marked  improvement 


Anesthesia  is  usually  present.    Hysterical  symp- 
!  not  abolished  during  the  attack  as  may  occur  in  epilepsy  (1058). 

rertigo  and  vomit- 
lilar  attacks  with- 
:  lesions  in  the  cerebral  cortex. 


Stokes-Adams'  Disease,  (430,  1057). 
Anemic  convulsion. 

Lead  convulsion  (494,  576,  1050). 
Alcoholic  convulsion,  (576,  658,  663,  764). 
Hysterical  convulsion,  (1074). 


Cerebral  Tumor  (including  abscess  and  cyst)  in  or 
near  motor  area  of  cortex.  Jacksonian  Epilepsy. 
(431,  507-8,  605.)     (Figs.  15-16.) 

Hemorrhage  in  or  near  motor  area  of  cortex  (pachy- 
meningitis, etc.).     Jacksonian  Epilepsy. 
(502,  1060.)     (Figs.  15-16.) 


after  some  prodromal  symptoms  such  as  headache,  poor  eyesight,  etc., 

y,     (By  lumbar  punct ure,  Weichselbaum's  diplococcus  almost  always,  o 
:d    I      (Weichselbaum's  diplococcus).    Strong  retraction  of  head. 


n  persons  who  have  been  exposed  to  high  temperatures.    Delirium  is  usually  present, 
rarely  the  pneumococcus  or  other  germs,  may  be  found  in  the  cerebrospinal  fluid.    There 


Sunstroke  i 


epidemic  of  the  dis 


Heatstroke,  (966,  1068). 
1214, 


Cerebrospinal  Meningitis, 
1226). 


By  lumbar  puncture,  pyogenic  bacteria  may  be  found  in  the  cerebrospinal  fluid.    Suppuration  or  an  infected  wound  may  be  present,  especially  in   the  head.    Suppurati. 
[      or  in  nasal  sinuses,  carbuncle  or  erysipelas  of  head  or  neck.    Retraction  of  head  may  be  less  marked. 


liddle  ear  or  mastoid,       Purulent  Meningitis,  (1227). 


ob-  By  lumbar  puncture  tubercle  bacilli  may  be  found  in  the  cerebrospinal  fluid.     A  tuberculous  process  may  be  found  in  some  other  part  of  the  body.     Gr! 

ho-  Choked  disc  and  choroid  tubercles  may  occasionally  be  seen  by  ophthalmoscopic  examination.     Tuberculin  skin  test  will  be  positive. 

ite, 

der  By  lumbar  puncture  no  bacteria  can  be  found  in  cerebrospinal  fluid.    Many,  if  not  all,  of  the  general  symptoms  of  meningitis  may  be  present,  but  they  i 

of  as  in  the  other  forms  and  are  promptly  relieved  by  the  withdrawal  of  a  moderate  amount  of  the  cerebrospinal  fluid. 


rig  of  teeth  and  hydrocephalic  cry.       Tuberculous  Meningitis  (1228-9). 


:  not  so  severe  and   are  not  so  constant 


ecting  the  nervous  system. 

of  intestinal  putrefaction  and  other  abnormal  processes,  often  started  by  the  ingestion  of  tainted  meat  and  other  poisons.     Vomiting,  tympanites,  diarrhoea  and  foul  smelling  feces. 


Serous    Meningitis,    Meningismus. 
(1239). 


Febrile  or  toxic  convulsion 
Auto-toxic  convulsion,  (576,  1067). 


CHART  XI  b 

Clonic  or  Tonic  Spasm 

Comprising  Numbers  ">72  on  left  side  of  Chart 
and  600  to  621  on  right  margin 

(Note) — Many  of  the  spasms,  especially  the  tonic  spasms,  are  associated  with  pain,  and 
are  then  called  "cramps." 


1:1: 


DIAGNOSTIC  SYMPTOMS  AND   TESTS 


571 

L 

Pyrexia  in  very 

O 

acute  cases. 

C 

C 

L 

A 

0 

"NT 

L 

JN 

I 

c  ■ 

c 

L 
0 

s 

N 

p 

I 

A 

C 

S 

Apyrexia 

M 

s 
p 

A 

572 

T 
O 

N 
I 
C 


Pyrexia 


L 

O 

c 

A 
L 

T 
0 
N 
I 

c 

s 
p 

A 

S 

I    M 


A  pyrexia. 


Shock-like   spasms   similar  to   that    pro- 
duced by  an  electric  shock 


Begins  in  one  arm  and  side 
.side  and  then  to  opposite 


A~single]_or  many 
times  repeated 

spasm,  rarely  con- 
tracture, of  one 
muscle  or  of  a 
group  of  muscles, 
occurring  in  parox- 
ysms which  rather 
tend  to  subside  on 
voluntary  move- 
ment s.  Myoclonus. 
(270.) 


Spasm      commenc- 
ing in  jaws. 


Spasm  commenc- 
ing in  pharynx  and 
oesophagus. 


'Occurs  in  face  and  more  rarely  in  neck      The  s 
and  arms.  am 


Begins  in  arms  and  may  extend  to  legs,      The 
but    almost  never  to  face.     Often  the  mi 

tendons  play  as  in  subsultus  tendinum.  ax< 


Begins  in  side  of  face  or  in  one  arm  or  The 
leg  and  may  extend  over  one,  or  even  fir: 

both  sides  of  body. 

There  is  the  history  of  anrinfected  wound,  or  septi 
of  jaws,  occurring  in  paroxysms;  also  rigidity  t 
body  being  held  in  posilion  of  opisthotonus,  on 
becomes  very  high.    The  disease  varies  greatly 

There  is  history  of  a  bite  by  an  animal  (usually 
especially  on  sight  of  water.    Spasmodic  closur 
cough,  opisthotonus  and  general  spasm  are  cor 
light  and  accommodation.    The  stage  of  excitt 
diagnosis  must  be  made  in  such  cases  by  the  I 


Spasm  commences  in  back  of  neck  and 
in  back. 


There  may  be  more  or  less 
symptom.     Lumbar  pui 

fThe 


Apyrexia.  If  un- 
consciousness i  s 
present.  See  also 
epilepsia  media 
1(575). 


'Cerebellar      ataxia 
is  present  (281). 


A  tonic  spasm  of  sudden  onset,  the  face    \ 
not  being  affected. 


dell 
Retr 


Extremities  and  trunk  rem 
attack  may  last  minutes 


Rigidity  rather  than  spasm,  not  strong 
enough  to  prevent  passive  or  volun- 
tary movements  (266). 

(Rigidity  of  all  muscles,  mr 

Spasm  passes  away  as  the  action  is  continued,  to 
the  muscles  of  the  face  usually  escape  altogetl 
fibers  show  marked  hypertrophy.  Closely  alii* 
low  exposure  to  cold  with  consequent  rellcx  VI 
The  so-called  acquired  form,  "  myotonia  acqui 

Bilateral  painful  tonic  spasm  of  muscles  of  hands 
tended.  Increased  mechanical  (Trousseau's  pi 
dated  with  rickets  or  digestive  disorders  and  i 
It,  occurs  in  infectious  diseases,  in  poisoning  a; 

General  painful  clonic,  followed  by  tonic,        Spasm  very  general  and  v 
spasm.  ni,,'c  poisoning.  Death  h 

General  permanent  contracture.  Paralysis  is  coincident  will 

Spasm  only  occurs      Occurs  usually  in  small  muscles  and  in  those  Iha 
when       performing  gradual  onset,  steadily  grows  worse,  and  rendei 

some  accustomed  rather  than  spasm.     Atrophy  of  the  muscles  i 

act,  the  voice  of  singers,  public  speakers,  etc. 


Spasm  only  at  com- 
mencement of  any 
action. 


Spasm  mainly  con- 
fined to  hands  and 
feet,  paroxysmal. 


Rather    brief    spasm 
muscles. 

More   permanent 
spasm. 


A  permanent  or,  at 
least,  a  long  con- 
tinued, contracture. 
The  muscles  are 
anatomically  short- 
ened, i  n  later 
stages. 


of    one    or    more       A  spasm  lasting  minutes  < 
cough,  oesophageal  spas 

A  contracture  of  a  few  or  many  muscles  usually 
efforts  are  made  to  overcome  it.  No  muscle  at 
bling  (674)  or  may  consist  in  jumping  or  ski  I 

A  hemiplegic  con-  fTendon  reflexes  air  incrflG 
fracture.  i      and  lasts  for  years.    Usi 


A    paraplegic    con- 
tracture. 


I  Tendon  reflexes  are  increaijl 
I     follows  an  attack  of  par 


A  local  contracture.       Absence  of  reflexes.     Muel  i 
^     traction  of  tendon  and  I 


DIAGNOSTIC   ANALYSIS   OFf  SYMPTOMS 

ABSTRACTS  OF  SYMPTOMS 


ck  and  extends  to  leg  of  same      Much  pain  in  head  and  neck  at  onset.    Weakness  slowly  follows  the  spasms.    At  times  there  is  wastin 

spasms  become  violent  ar.d  more  continuous.     Epileptiform  attacks  are  common.     Death  results  in  a  few  nlonths 


uscles  and^loss    of    faradic    excitability.     The      Dubii 


DIAGNOSIS 
Electrical  Chor. 


s  are  almost  always  unilateral, 
ri  bilateral  are  not  symmetrical. 


is  are  bilateral  and  fairly  sym- 
,  but  not  synchronous.  They 
-ular  in  force  and  rhythm,  and 
lost    always    limited    to    one 


The  spasms  seem  like  mimic  gestures  and 
appear  to  be  rather  purposeful.  May 
have  originated  from  local  irritation,  but 
have  persisted  after  the  irritation  has 
ceased. 

The  spasms  never  appear  to  be  purpose- 
ful. No  movement  results,  merely  indi- 
vidual muscles  spring  forth  in  strong 
contraction.  Irritation  of  the  skin  or 
tendons  causes  paroxysms. 


ychic    disorders    of    an    emotional    or 
neurasthenic  nature  often  present. 


The  contractures  ; 
(617). 


:  accompanied  by  no  pain. 


i  also  reflex  spasm      Convulsive  Tic    (blepharospasm,    torticollis,    etc.),     601 
(267,  270,  617,  726). 


The  contractures  are  accompanied  by  sharp  darts  of  pain, 
emotional     disturbances,  f  The  muscles  involved  are  attached  by  one  end  to  the  trunk  < 


Trembling    of    muscles    between    the 
paroxysms.      The    spasms  become  ler~ 
or   entirely   cease,  during   sleep.      E 
irated. 


Muscles  of  the  face,  hand  and  forearm,  foot  and  lowe 
never   involved.    No  heredity.     A  disease  of  adult  life. 


Many  cases  occur  in  the  same  generation  of  a  family, 
begins  in  early  life  and  is  associated  with  epilepsy  and  i 


are    always    unilateral    at      The  spas 


may  extend  to  adjacent  muscles  and  so  over  one  half  the  body  and  then  pass  across  and  involve  both  sides,  or  it  may  remain  a  ocal  spasm  and 
V  in  a  short  time.  After  many  such  local  spasms,  one  may  occur  which  will  pass  into  a  general  convulsion.  A  general  convulsion  can  some- 
times be  averted  by  tying  a  band  tightly  around  the  extremity  as  soon  as  the  local  spasm  appears  Consciousness  is  always  lost  when  the  convulsion 
extends  to  both  sides  of  the  body;  but  usually  persists  when  spasm  is  limited  to  one-halt  the  body  or  to  one  extremity, 
lbirth  within  a  month  usually  within  two  weeks.  The  infection  may  occur  through  the  navel  in  new  born  babies  (tetanus  neonatorum).  The  characteristic  symptom  is  rigid  spasmodic  closure 
1  ,  «,  k ,  .  1  ,  cmE "  nsus saXiicus  "  In  the  onset  a  gradually  increasing  stiffness  of  masticatory  and  other  muscles  followed  and  accompanied  by  paroyxsms  of  painful  tome  spasms; , he 
Clonus  pieSrosthd"onus  d, ^  orthotonus  (265).  The  spasms  are  associated  with  profuse  sweating.  There  are  no  mental  symptoms  and  no  coma.  Towards  the  fatal  termination  the  temperature 
ensity.   '  The  longer  the  incubation  period  the  milder  the  disease.    Local  tetanus  and  head  tetanus  with  local  paralysis  have  been  described. 

■  cat)  within  a  year  usually  within  six  months.  The  most  striking  features  are  tremor,  rapid  pulse,  fever,  mental  depression,  fright,  horror  and  extraordinary  emotional  excitement,  even  mania, 
harynx  ad Oesophagus  mldng swallowing,  especially  of  fluids,  impossible.  Saliva  cannot  be  swallowed  and  is  expelled  from  the  mouth  with  difficulty.  Spasm  of  muscles  of  respiration,  hie- 
Eeflex  acirtrom  cutaneous  or  special  sensory  surfaces  are  greatly  increased,  especially  that  of  inspiratory  dyspnoea;  and  priapism  occasional!*  occurs.  The  pupils  are  dilated  and  respond  to 
is  aftlmes  followed lb} 'a  si "age  of  paralysis  and  is  often  preceded  by  a  prodromal  stage  of  malaise  and  of  pains,  especially  in  the  scar.  Hysterical  persons  at  times  simulate  hydrophobia.  Ihe 
:e  of  hysterical  symptoms  (425),  absence  of  fever  and  by  time. 

rbance,  or  loss,  of  consciousness.    Tonic  retraction  of  neck,  opisthotonus  and  boat-shaped  retraction  of  abdomen.     Slight  irritation  will] cause,  s; 
shows  increase  of   cells  in  cerebro-spinal  fluid ,  except  in  serous  meningitis.     For  different  varieties  see  590-4. 

nities  on  the  same  side  as  the  lesion  are  adducted,  on  the  opposite  side  abducted.     Head,  trunk  and  extremities  each  rotate  about  long  axis  fro\ 
towards  the  same  direction. 

of  the  head  and  opisthotonus,  flexion  of  elbows,  supination  of  hands,  extension  of  legs  with  pointing  of  toes. 


Tic  Douloureux,  (267,  726,  947).  602 

Friedreich's  Paramyoclonus  Multiplex.  603 

Unverricht's  Family  Myoclonus  Epilepticus.  604 

Jacksonian  Epilepsy,  (431,  587,  1282-3,  1291).  605 


Tetanus,    (170).      Tetanus   traumaticus.      Tetanus     606 
rheumaticus.       Tetanus     puerperalis.       Tetanus 
neonatorum. 


,  any  position  in  which  they  may  be  placed  for  a  surprisingly  long  time.  Wax-like  resistance  to  passive  motion.  Difficult  positions  mainta 
s  or  days.    Anesthesia,  abolition  of  reflexes,  and  apparently  more  or  less  complete  loss  of  consciousness  are  usual  symptoms.    Other  hysterical  " 

e  face,  speech  monotonous,  passive  tremor  of  hands  and  legs,  characteristic  attitude,  festinating  gait.  Tendency  to  fall  backwards  or  forwards 
l  on  first  movement  after  a  rest  or  when  action  is  done  faster.  Patient  cannot  hurry  or  execute  rapid  movements.  Is  liable  to  lose  equihbnu 
ilarked  heredity.     Myotonic  electrical  reaction  (402).     Increased  mechanical  excitability  of  muscle,  even  slight  pressure  wilh  the  finger-tip  causei 

his  disease  is  "paramyotonia  congenita"  (Eulenberg's  disease)  also  on  an  hereditaiy  basis  (it  has  attacked  twcniy-eight  members  of  a  family  inr 
itor  spasm  and  nutritive  disturbances  in  the  muscles.     A  myotonia  congenita  intermittens  and  a  myotonia  congenita  atrophica  have  been  descnb 

is  probably  an  altogether  different  disease. 

sometimes  of  feet,  lasting  minutes,  hours,  or  rarely  days.    Hands  and  feet  drawn  into  smallest  volume    possible  with  hollow  deepened  (obstet 
enon  (450))  and  electrical  (Kill's  sign  (452))  excitability  of  nerves.     Facial  nerve  very  irritable;    so  that  slight  blows  on  it  cause  spasm  of  facia 
lal  parasites,  or  dilated  stomach;  often  follows  extirpation  of  parathyroid  glands.     Sometimes  occurs  as  a  symptom  of    hydrocephali 
pregnancy  and  as  an  occupation  neurosis  (616).      In  some  cases  this  disease  may  be  due  to  destruction  of  the  parathyroid  glands  and 
linful,  mainly  in  the  form  of   opisthotonus  (265).    Periods  of  intermission  with  relaxed  muscles  lasting  several  minutes.    Cutaneous  and  tendon 

results  in  a  couple  of  hours.  u-ii.iv; 

contracture.  Convulsions,  mental  defect  and  partial  arrest  of  growth,  are  common.  The  contracture  and  motor  paralysis  may  be  unilateral  or  D 
1  been  overworked  or  improperly  worked  in  doing  the  same  act  many  times.    The  spasm    is  often  painful,  and  in  some  cases  pain  may  be  the  c 

accustomed  act  difficult  or  impossible.     It  occurs  only  when  the  muscles  are  used.    In  some  cases  there  is  tremor,  in    others  ^incoordination 
ed  is  common.     Patients  are  usually  neurasthenic.     Many  varieties:  writer's,  telegrapher's,  pianist's,  violinist's,  seamstress,  shoemakers, 


ned  indefinitely  without  apparent  effort, 
s  jrmptoms  are  often  present,  (425). 


ebra  I 

y  peihaj 


Headache,   backache,   delirium,   Kernig's 


;ide  of  lesion  to  the  opposite  side  and  the  eyes 


577). 

The  arms  are  less  affected  than  the  legs  and 
sluggish  long  continued  contraction.     Muscle 
generations),  but  these  paroxysmal  attacks  fol- 
1  with  the  characteristics  implied  in  their  names. 


Hydrophobia.     Lyssa.     Rabies,  (171). 


Meningitis,    Cerebral   and    Spinal,    (508,    590, 
831,  974,  1005,  1032,  1045,  1208-9-13). 

Lesion  of  cerebellar  hemispheres, 
(648,  686,  783,  1016,  1272). 

Lesion  of  vermis  of  cerebellum, 

(648,  686,  7S3,  1016,  1272). 
Catalepsy,  (1096-8). 

Paralysis  Agitans.     Parkinson's  disease, 

(677,  766,  800). 
Myotonia    Congenita.      Thomsen's    disease, 

(265,  1155),  including  Paramyotonia  Congenita 

(Eulenberg's  disease). 


irs,  due  to  local  irritation  in  neurasthenic  patient 
ethral  spasmodic  stricture,  vesical  spasm,  t 


Functional  in  its    nature.    Many  varieties.     Blepharospasm,  torticollis,  spasmodic  croup,  la 
etc.    See  also  the  convulsive  tics  (601). 

liated  with  anesthesia  of  the  part.  Usually  there  is  a  combination  of  spasm  of  flexors  and  extensors,  such  as  is  not  seen  in  organic  disease.  A  f 
if.  At  times  may  be  cured  by  ovarian  pressure  or  by  faradization.  Other  hysterical  symptoms  (425).  Hysterical  spasms  are  not  always  in  the 
;  (saltatory  spasm). 

■hen  the  spasm  does  not  prevent  their  occurrence.  Little  or  no  muscular  atrophy.  The  spasm  is  limited  to  the  arm  and  leg  of  the  same  side  a 
there  are  flexion  of  elbow,  wrist  and  fingers,  and  extension  of  knee.     Is  associated  with  a  sclerosis  of  the  pyramidal  tract  and  indicates  a  hopeless 

hen  the  spasm  does  not  prevent  their  occurrence. 
a.     It  is  of  very  bad  prognosis. 

icular  atrophy.     Is  limited  to  the  distribution  of  one  i 
rather  than  of  muscle. 


(hand).    Joints  of  arms  flexed,  those  of  legs  ex-      Tetany,  (120,  616). 
muscles  (Chvostek's    sign  (4.51)).     Usually  asso- 
umor  or  other  serious  brain  disease  in  children. 
,  be  cured  by  the  administration  of  these  glands, 
flexes  increased.    History  or  evidence  of  strych- 

iateral. 

ly  symptom  (neuralgic  form).     The  spasm  is  of 

rare  cases,  paralysis  or  paresis  (paralytic  form) 

lamp.       A  similar  neurosis  occasionally  affects 

aus  stridulus,  bronchial  asthma,  whooping 


Strychnine  convulsions.  (314-7,  3( 

Cerebral  palsy  of  childhood, 
(116,  501,  577,  630,  79S,  1048). 

Occupation  Neuroses,  (143,  614). 


615 

615a 


ctional  spasm,  which  becomes  greater  the  more 
of    contracture.     They  may  consist  in  trem- 

follows  an  attack  of    apoplexy,  by  a  few  weeks 
gnosis  as  to  recovery  from  the  hemiplegia. 

Little  or  no  muscular  atrophy.    The  spasm,  which  is  often  not  so  continuous  as  in  the  hemii     »ic  form,  consists  in  flexion  of  both  knees,  and 


more  nerves.    Folio 


of  nucleo-peripheral  moto 


Occurs  in  fingers. 


puytren's  contracture  seems  to  be  due  to  con- 


Reflex  spasm,  (601,  637,  1194).  617 

Hysterical  contracture,  (1074).  618 

Post-hemiplegic  contracture,  (501,  504,  577,  615a).  619 

Post-paraplegic  contracture  (512-20,  548-51,  795).  620 

Post-neuritic    contracture.      Dupuytrcn's    contrac-  621 
ture. 


i 


CHART  XI  c 

Choreiform  and  Athetoid  Spasms 

I  lomprising  Numbers  ~>~'-'<  and  57  I  on  [efl  ride  of  <  Ihari 
■Mill  622  i"  ii:;i  on  right  margin 


I3U 


CHART  XII 

Perversion  of  Motion 

and 

Local  Palsies  and  Spasms 


DIAGNOSTIC  ANALYSIS  OF  SYMPTOMS 


Symptom  Analysed  Character 

-638 
ATAXIA  (248) 


635 
PERVERSIONS 

OF  MOTION 

(243) 


639 

TREMOR  (250) 

640 

NYSTAGMUS  (291) 

641 

FIBRILLARY  CONTRACTION 
OR  FIBRILLATION  (292) 


The  diseases  in  which  ataxia  occurs  are 
set  forth  in  Chart  XII  a. 


The  diseases  in  which  tremor,  nystagmus, 
or  fibrillation  occurs  are  set  forth  in 
Chart  XII  b. 


636 

LOCAL  PALSIES 


637 

LOCAL  SPASMS 


LOCAL  PALSIES  AND  LOCAL  SPASMS 

See  Chart  XII  c. 
See  Chart  XII  d. 


141 


CHART  XII  a 

Ataxia 

Comprising  Numbers  (ills  and  642  to  64  I  on  left  side  of  Chart 
and  648  to  664  on  right  margin 


L43 


DIAGNOSTIC  SYMPTOMS  AND  TESTS 


63 
A 

T 
A 
X 

1 

A 
(248) 


642 

Ataxia  mainly 

upon    standing  ,'  or 
walking.     Stagger- 
ing   gait. 
Static  ataxia. 
Cerebellar  ataxia. 
(281). 


043 

Inability  to  stand 
or  walk.  More  or 
less  complete. 


No  loss  of  muscle 
sense.  No  motor 
paralysis,  except  in 
late  stage  of  651-2. 


f  Bilateral. 


Unilateral. 
I  (Hemiataxia  ) 


^Unilateral. 
(Hemiataxia.) 


044 

Ataxia  of  all  move- 

mei.  -j  Bilateral 

Dynamic  ataxia. 

Motor  ataxia  (280  j. 


Irregular 
^-distribution. 


("Occurs  at  any  age, 
usually  in  adults. 

I  Usually  sensory 
symptoms 


Occurs  in  youth. 
No  sensory  symp- 
toms. 

Many  sensory 
symptoms. 

Often  analgesia 
and  thermic 
anesthesia. 


Sight    and    hearing 
normal. 


Sight     or     hearing 
abnormal. 


Patient  e; 
nystaga  ; 
Hypotoi 
very   mi 

mally. 
at    time 
normal. 

Occurs  in  family  groups  and  si 
though  less  pronounced.  A  ge 
mus  is  common  and  speech  oi 


(230)  r; 

No  loss  ol 
lying  dc 


Evidently  func- 
tional. 

Evidently  organic. 


Loss      of      muscle      When  of  acute  course  the  condi 


sense  and  sensory 
symptoms  usually 
prominent.  Knee- 
jerk  usually  in 
creased. 


ally  follows  an  apopleci  ic  atl  Si 
arterial   disease   is   pre 
chronic    course    choked    disc 
present. 


Knee-jerks  normal.    No  ankle-clonus. 


History  c 


("Great  variety  of  local  symptom 

are  intention  tremor,  Bcanrjnf 

I      ness.     Rarely  the  disease  run 

J     essential  point  is  the  presenc< 

A  combination  of  symptoms  of 
usually  lost  before  any  anrstl 
Knee-jerks  may  be  abolished 

"Rarely  any  permanent  motor  p; 
ball)  are  not  uncommon  earn 
held  well  apart  and  feet  are  fl 
symptom  (448), Argyll-Robert: 
sensations  and  paresthesias  a 
gesia  in  patches  and  in  cuirat 
in  cerebro-spina]  Quid.  The  i 
Positive  Wassermann  also  urn 
mainly  affected.  In  the  ordii 
and  the  diagnosis  must  rest  m 

Slight  motor  paralysis  is  presen 
normal.  Cranial  nerves  rarer 
never  so  chronic  as  tabes.    Ni 

Knee-jerks  usually  exaggerated,  but  no  J 
Babinski  or  ankle-clonus.  Evidently  ■< 
functional  (pseudo-ataxia).  [  j-;,,10ti0nal 


Exaggerated  knee- 
jerks,  ankle-clonus 
and  Babinski. 


Knee-jerks  and  an- 
kle-clonus absent. 
No  Babinski.  Often 
loss  of  muscle  sense 
and  retardation  of 
conduction  of  pain. 


DIAGNOSTIC  ANALYSIS  OF  SYMPTOMS 


ABSTRACT  OF  SYMPTOMS 

s  the  staggering,  irregular  gait  of  a  drunken  man.     Little  ataxia  of  movements  of  hands,  or  of  legs  when  lying  down.     Vertigo,  vomiting  and  headache  are  often  present.     Choked  disc  or 

nay  be  present  (tumors').     Knee-jerks  may  be  present  or  absent  (usually  present).    Cerebellar  fits  (609-10)  may  occur.     Symptoms  may  be  bilateral  or  unilateral  (same  side  as  lesion). 

i  present, also  a  diadocokinesia  (36)  due  fcoalong  continuanceof  muscular  contraction.     Patients  can  he  on  back  with  legs  flexed  at  hips  and  knees  much  longer  than  a  normal  person  and 

onger  than  patients  with  dynamic  ataxia. 

t,  constantly  or    paroxys-    f  Diplopia  or  other  disorders  of  sight.     Vertigo  ceases  when  eyes  are  closed. 

lache,  vertigo  and  vomiting    < 

:>  choked  disc.    Knee-jerks    [  Deafness  and  ringing  in  one  ear.    Paroxysmal  attacks  of  intense  vertigo  and  defect  in  bone  conduction  are  frequent  symptoms. 


well  marked  heredity  usually.  Staggering  gait,  but  ataxia  also  in  armsj 
,  coarse,  irregular  tremor,  simuhil  ing  jerky  choreiform  movements.  Nystag- 
iefective.    Symptoms  present  a  mixture  of  weakness  and  ataxia. 


Occurs  after  puberty.      Knee-jerks  present.     Ocular  paralysis,  loss  of  pupil  reflex  and  optic  atrophy  common. 

early  stage   and    in  exceptional  cases.    Babinski  reflex 
power.      Simulates  an  apraxia 


Occurs  before  puberty.     Knee-jerks  absent,   except 
usually  present.     Optic  atrophy  rare.     Club-foot 

loved  easily  in  all  directions  without  ataxia  when  patient  is  lying  down,  but  collapse  when  she  tries  to  walk,  apparently  from  lack  of  confidence  and  w 
than  an  ataxia.    Often  has  an  emotional  cause  and  hysterical  symptoms  (425)  are  present.    Both  legs  are  involved. 

icle  sense.    May  or  may  not  be  motor  paralysis  of  same  side  with  analgesia  and  thermic  anesthesia  of  contralateral  side.     One    leg    only  involved.     No    ataxia    when 
but  marked  ataxia  while  walking 


leg  while 


Marked  anesthesia  without  analgesia.    No  motor  paralysis.     No  other  symptoms.     Very  rare.     May  be  the  earliest 


Apoplecf iforrn  attack  followed  by  hemiplegia  (sensory  oftener  than  motor).    Other  post-hemiplegic  motor  disturbances  are  often  present.     The  ataxia  occur 
cases  where  the  motor  paralysis  wras  slight. 


spinal  tumor.     Unilateral  later  becoming  bilateral. 
conv;dL'scence  in 


be    j  There  are  often  ataxia  and  loss  of  muscle  sense  on  one  side  of  body  and  analg 
I      arthria  and  paralysis  of  various  cranial  nerves  are  usually  present. 


.  and  thermic  anesthesia  on  the  other  side.     There  may  be  crossed  paralysis.     Dysphagia  and  dya- 


LSigns  of  cortical  irritation  (convulsions).    Anesthesia,  especially  loss  of  muscle  sense,  is  often  present.    Headache  common.    May  be  some  mental  disturbance. 


•  Imli- 


Blurred  and  foolish  speech.     Ataxia  and  other  sympta 


Temporary  tremor. 


'sually  both  motor  and  sensory  symptoms.  Irregular,  jerky,  ataxic  movements  of  both  arms  and  legs,  and  movements  are  slow.  Gait  is  often  both  spastic  and  ataxic.  Very  characteristic 
;eh,  nystagmus,  especially  on  motion  of  eyeball,  and  atrophy  of  optic  nerve.  In  some  cases  bulbar  paralysis  (434)  is  an  early  symptom.  Patients  are  often  emotional  and  exhibit  mental  weak- 
acute  course  and  has  been  called  "acute  ataxia,"  of  which  there  are  several  varieties  (662).  In  its  early  stages  the  diagnosis  of  this  disease  is  often  exceedingly  difficult.  The  most 
lymptoms  only  explicable  on  the  assumption  of  the  existence  of  several,  separate,  small  lesions. 


motor  ataxia  (661)  and  spastic  paraplegia  (525)  in  varying  proportions.    Little  or  no  pain.     Weakness,  stiffness,  ataxia,  paresthesiae  and 
can  be  detected.     In  later  stages  arms  may  be  somewhat  involved.     A  rare  disease.     Occasionally  some  involvement  of  cranial  nerves.     Orga; 
rds  the  end  of  the  disease,  but  Babinski  persists.     This  disease  may  be  caused  by  pernicious  and  other  severe  anemias. 


of  legs.     Vibration  sense  (56,  353)  is 
reflexes  slightly,  or  not  at  all,  disordered. 


sis;  but  hypotonia  (252),  allowing  hyperextension  and  extreme  mobility  of  joints,  is  common,  and  temporary  paralyses  in  the  domain  of  the  cranial  nerves  (especially  the  muscles  of  eye- 
iptoms.  Movements  are  ataxic,  quick,  violent,  excessive  and  constantly  controlled  by  eyesight.  The  affected  parts  cannot  be  held  motionless  in  one  position  long.  In  walking,  legs  are 
too  far  outward  and  too  far  forward  and  are  brought  back  hard  on  heel.  Ataxia  much  worse  when  eyes  are  closed.  Walking  in  the  dark  or  backwards  is  usually  impossible.  Romberg's 
phenomenon  (447),  myosis  and  optic  atrophy  with  concentric  limitation  of  field  of  vision  are  common.  Lightning  pains  of  great  intensity  in  small  areas  followed  by  hyperalgesia,  girdle 
ominent  symptoms.  Organic  reflexes,  especially  the  vesical,  are  disordered.  Arthropathies  (11S6),  or  perforating  ulcer  or  other  trophic  disorders  may  be  present.  Anesthesia  and  anal- 
nar  hyperlhesia).  Retardation  of  conduction  of  pain.  Visceral  crises  (9S7)  are  usually  present.  Towards  the  end  of  the  disease  motor  paralysis  may  appear.  Lymphocytosis  and  globulin 
se  is  sometimes  divided  into  three  stages — (1st),  the  neuralgic;  (2nd),  the  ataxic;  (3rd),  the  paralytic  stage.  History  or  other  evidences  of  syphilis,  or  of  venereal  disease  is  usually  present, 
present.  There  are  several  forms  of  tabes.  In  the  cerebral  form,  atrophy  of  the  optic  nerve  is  the  prominent  symptom  and  the  legs  show  little  ataxia.  In  cervical  tabes  the  arms  are 
form  the  legs  are  mainly  affecled.  In  all  forms  the  knee-jerks  are  absent.  Babinski  is  present  in  rare  cases,  complicated  by  lateral  scleroses.  In  many  cases  of  tabes  the  ataxia  is  slight 
'  on  the  absence  of  the  knee-jerk,  the  Argyll-Robertson  phenomenon  and  the  cerebro-spinal  lymphocytosis,  together  with  whatever  other  symptoms  may  be  present. 

luscles  tender  and  atrophic.    Pains  rarely  very  severe  and  partial  reaction  of  degeneration  and  retardation  of  conduction  of  pain  often  present.     Organic  reflexes  normal.     Pupil  reaction 
rolved.     Usually  sensory  symptoms.     Usually  history  of  alcoholic  abuse.     Mental  disturbances  in  many  cases.     Occasionally  the  disease  runs  an  acute  course,  "acute  ataxia,"  (659)  and  is 
bulin  or  lymphocytosis  in  cerebro-spinal  fluid.    Prognosis  is  good, 
ing  drugs,  alcohol,  etc.  The  ataxia  is  usua 

and  excitable. 


?iated  with  tremor  and  neurasthenic  symptoms.    Failure  of  memory  and  other  signs  of  mental  impairment.    Patients  are  emotional 


The  ataxia  may  appear  only  when  eyes  are  closed  and 
but  usually  collapse  on  reaching  a  place  of  safety. 


usually  associated  with  cortical  anesthesia.     Hysterical  symptoms  (425)  are  present.     Rarely  fall, 


DIAGNOSIS 

Lesion  of  cerebellum  or  it;  tracts;  if  acute  in  onset,     648 
apoplexy;  if  chronic,   tumor,    (609-10,   654,   686, 
783,  1016,  1272). 

Ocular  ataxia  or  vertigo,  (1020).  649 

Aural  ataxia  or  vertigo.     Meniere's  Disease,  650 

(685,  91S,  1019). 

Marie's  hereditary  cerebellar  ataxia,  651 

(669,  782). 
Friedreich's  Disease.    Hereditary  Ataxia,  652 

(670,  6S7,  762,  781). 
Astasia  and  Abasia,  (2S7,  792).  653 

Lesion  of  lateral  column  of  spinal  cord,  involving     654 

direct  cerebellar  tract,  (64S,  1356,  1360,  1396). 

(Figs.  24-7.) 
Lesion  of  posterior  column   of  cord,  (785,  1350-1     654a 

1347,  1396).     (Figs.  24-7.). 
Post-hemiplegic  ataxia  (lesion  in  or  near  posterior     655 

part  of  optic  thalamus  (1275).     (Fig.  17.) 

Softening,  hemorrhage  or  tumor  in  brain  srem,  656 

(535  et.  seq.,  S30,  1268-71).    (Figs.  19-22.) 

Softening  or  tumor  of  contralateral  parietal  cortex.      657 

(1355,  1362).     (Fig.  15.) 
Alcoholic  intoxication,  (663,  673,  764,  780).  658 

Disseminated  Sclerosis.   Myelitis  Disseminata.  659 

Encephalomyelitis,  (511,  580,  668,  688, 

756,  765,  799,  913,  1051). 


.taxic  Paraplegia.     Combined  Sclerosis, 
(526,  796).     (Figs.  24-6.) 


Locomotor  Ataxia.    Tabes  Dorsalis, 

(433,  756,  784.  827,  894,  979,  987,  1004,  1217, 
1231).     (Figs.  24-6). 


Multiple  Neuritis.  Polyneuritis.  Pseudo-tabes, 
(4S8,  787,  823,  1008,  1147,  1307) 

Drug  habit  (toxic),  (482,  658,  764,  7S0). 
Hysterical  Ataxia,  (1074). 


CHART  XII  b 

Tremor,  Nystagmus,  Fibrillation 

Comprising  Numbers  <>:i'.i  t<>  647  on  left  side  of  Chart 
and  litis  in  697  on  right  margin 


II.'. 


DIAGNOSTIC  SYMPTOMS  AND  TESTS 


o:?9 

T 

R 

E 

M 

0 

R 
(250) 


640 
N 
Y 
S 
T 
A 
G 
M 
U 

s 

(291) 


■645 

Intention 
290). 


646 

Passive  Tremor.  In- 
creased   on    volun- 
J  tary    motion    a  n  d 
excitement  (289). 


G47 

Passive        Tremor. 

Diminished         o  □ 

voluntary      motion 

(289). 


fC'oarse,  irregular 
tremor;  4  to  8  per 
second. 


Fine  tremor. 


Pine,  rapid  tremor;   « 
S  to  12  per  second.    | 


Slow  tremor;  3  to  G 
i  it  second. 


Slow,    fine   tremor; 
3  to  G  per  second. 


Tremor  is  usually  associated  with  scanning  speech,  nystagmi 
Usually  a  greal  variety  of  motor  and  sensory  symptoms  d 
sionally  with   their  loss,  over  a    very  variable  area.    The  i 
Vertigo  is  a  very  common  symptom. 

Occurs  in  family  groups  and  shows  well    I  Oecurs  after  pul 
marked     heredity.       Staggering    gait,  j 
Ataxia.      Nystagmus   is   common   and  1 
speech   often   defective.  [  Occurs  before  pu 

Tremor  is  associated  with  general  weakness  or  convalescence 

Exopblhalmus,  goitre,  tachycardia,  vascular  throbbing,  Bus 
when  patient  looks  downward  (Graefe's  symptom).     The  g 

History  of  addiction  to  alcohol  or  drugs.     .Menial  symptom* 
greatly  at  different  t  imes. 

Presence  of  hysterical  symptoms  (425).    Tremor  is  worse  wh 

Tremor  is  marked  in  fare,  lips  and  tongue.     Progressive  roei 
cytcsis  and  globulin  in  cerebro-spinal  Quid.    Wassermann  i 


Slow,  coarse 
tremor. 


Either  Intention  or  Passive  Tremor. 


Always  a  symptom 
of  organic  disease. 
Very  rarely,  an 
hysterical  clonic 
spasm  may  simu- 
late true  nystag- 
mus (pseudo-nys- 
tagmus). This  is 
often  vortical  and 
is  more  rapid  and 
more  violent  than 
nystagmus  and  is 
associated  w  i  t  h 
other  hysterical 

symptoms  (425). 


'No  weakness  of  any 
rectus  muscle. 


Weakness   of  one  or 
muscles. 


Slow  tremor  of  hand  and  foot  of  same  side,  associated  with  ( 

Tremor,  which  is  associated  with  muscular  rigidity  and  mask-li 
involves  the  other  side.  The  tremor  is  mi  si  marked  in  tin 
acteristic  attitude  (head  and  body  bent  forward,  elbows  lit 
ilar  tendency  to  run  backwards  (retropulsion).     The  attitu 

The  disease  often  commences  with  a  stiffness  and  slowness 

no  sensory  symptoms  except  the  set  sation  of  rigidity  and 

Tremor  begins  bilaterally.     Head  is  early  affected.    Nodding 

Rotatory  or  nodding  tremor  of  head  occurring  suddenly  in  ri 
involved.     The  tiemor  ceases  when  the  child's  eyes  are  clo 

A  scries  of  jerky  tremors  limited  to  the  back,  or  involving  al 

Not  associated  with  other  nervous  symptoms.     Hereditary  b 

f  Defective  vision  from  whatever  cause, 

{  Due  to  lack  of  pigment  in  iris,  choroid 

(  ^Yorkers  in  mines.     Due  to  working  ii 

Paroxysmal  at  tat 
violently,  or  ga 

.  Vertigo,  cerebellfl 
Coarse,    jerky    tre- 
mor is  a  prominent   j  Occurs  in  early  y 
symptom.      Ataxia  j 
is  also  present.  I  Occurs  at  any  ag 

Cerebral  symptoms      occurs  in  mening 
present . 

Rickety     baby     in      Most  marked  whi 
winter.  ing  of  the  heat 

,  Congenital.  Lateral  oscillating 

more   of  the  recti       Nystagmus  occurs  in  convalescence  frc 


Impairment  of 
sight. 


No   impairment    of  ■ 
sight. 


Vertigo  is  a  prom- 
inent symptom. 


641 

FIBRILLARY  CON- 

Ti:  \i  in  in  in: 
FIBRILLATION 
(292  . 


Evidence  of  organic 
disease.  Degenera- 
tion of  peripheral 
motor  neurons. 

Evidence  of  func- 
tional not  organic 
diseases. 


Marked       muscular 
atrophy  with    muS-    - 
cular  weakness. 


No   muscular  atro- 
phy or  weakness. 


'Marked    sensory 
symptoms. 


Analgesia  and  the 

f  Muscular  atrophy 

No   sensory   symp-  {  Mllscular  ,tril|,iiy 
toms.  r  J 

[  Muscular  atrophy 
Occurs  usually  in 


DIAGNOSTIC  ANALYSIS  OF  SYMPTOMS 


ABSTRACT  OF  SYMPTOMS 

phy  of  optic  nerve  and  ataxia.  Reflexes  are  usually  exaggerated  and  ankle-clonus  and  Babinski  are  present.  In  some  cases  the  deep  reflexes  are  early  abolished  and  the  organic  reflexes  disordered, 
lany  local  lesions,  alt  In  nigh  all  these  may  be  absent.  The  motor  symptoms  commence  as  fatigue,  slowly  becoming  paresis,  rarely  paralysis,  and  are  usually  associated  with  exaggerated  reflexes,  occa- 
r  symptoms  are  usually  in  the  form  of  paresthesiae,  more  rarely  pain  followed  by  irregular  patches  of  anesthesia.     Epileptiform  or  apoplectiform  attacks  followed  by  transitory  paralysis  are  common. 

Knee-jerks  are  present.     Ocular  paralysis,  loss  of  pupillary  reflex  and  optic  atrophy  are  common. 

Knee-jerks  are  absent  except  in  early  stage  or  in  rare  and  exceptional  cases.     Babinski  is  present.     Optic  atrophy  rare.     Club-foot  common.     Rarely  sensory  symptoms  are  present, 
n  acute  disease.     Anemia  is  usually  present,  but  no  evidence  of  any  organic  disease  of  the  nervous  system.     Exhaustion  or  holding  a  limb  in  a  strained  position  for  a  long  time  causes  tremor. 

veating,  diarrhoea,  much  nervousness,  tremor  especially  marked  on  excitement,  polyuria  and  at  times  albuminuria,  insomnia  and  vertigo  are  common  symptoms.  The  upper  lid  does  not  fall  normally 
of  the  parenchymatous  variety  and  need  not  be  large. 

mmon,  moral  sense  and  judgment  impaired  and  speech  blurred.     Patient  is  restless  and  emotional.     Pupils  contracted  in  opium  cases.     Quinquand's  sign  (453)  in  alcoholic  cases.     Symptoms  vary 

ntion  is  directed  to  it.    Irregular  tremor.    Evidence  of  great  exhaustion  of  the  nervous  system.     Often  history  of  injury  associated  with  fright. 

History  of  syphilis.    Lumbar  puncture  shows  a  lympho- 


airment.     Eestless  and  childish.     Speech  is  slurred  by  elision  of  syllables  and  letters.    Apoplectiform  and  epileptiform  attacks  may  < 
usually  positive.     Argyll-Robertson's  phe: 


ator  paralysis  of  the  opposite  side.     Other  symptoms  of  a  severe  brain  Ie, 


May  be  associated  with  hemiplegia,  sensory  or  motor.     Tremor  ceases  during  sleep  and  i 


Teased  in  excitement. 


,  consists  of  "pill  re 
;  and  hands;  the  hi 

lees  slightly  flexes 
t  and  mask-like  fa 
ement  of  one 


novements  of  fingers  and  general  tremor,  which  commences  in  one  extremity,  later  extends  to  the  other  extremity  of  the  same  side  (rarely  to  that  of  the  opposite  side),  and  finally 
1  body  escape,  except  in  very  rare  cases.  Disease  commences  after  forty  years  of  age  and  progresses  slowly.  The  tremor  usually  becomes  coarser  in  the  later  stages.  Char- 
les! in;it  inn  Lr:iii  or  pp.pulMon:  a  tendency  to  fall  forward  winch  compels  patient  to  walk  faster  and  finally  to  run  until  he  falls  forwards  or  against,  an  obstacle.  He  has  a  sim- 
dl  due  in  inuscul.ir  rigidity  which  is  more  characteristic  of  the  disease  than  is  the  tremor,  and  in  rare  cases  occurs  alone  without  any  tremor  (paralysis  agitans  sine  agitatione). 
id,  simulating  a  mild  paralysis,  the  tremor  appearing  later.       Voluntary  movements  are  slow,  much  restricted  and  feeble,  but  are  never  completely  paralysed.      There  are 


of  heat,  which  are  frequent  and  distressing  symptoms.    Patient  slowly  becomes  entirely  helpless, 
tent.    No  rigidity.    General  weakness.    Atheromatous  arteries, 
tabies  in  the  winter  time  and  passing  off  in  the  summer  time.     Usually  accompanied  by  nystagmus  which  grows  worse  when  the  child's  head  is  held  still.      Occas 


ally   other    muscle    groups    are 


Multiple    Sclerosis.      Disseminated    Sclerosis, 
(511,  580,  659,  GSS,  756,  765,  799,  913,  1051). 


Marie's  Hereditary  Cerebellar  Ataxia,  669 

(651,   7S2). 

Friedreich's  Hereditary  Ataxia,  670 

(652,  6S7,  762,  7S1). 
Asthenic  Tremor  or  weakness,  (790).  671 

Exophthalmic  Goitre.    Basedow's  Disease.  672 

Graves'  Disease,  (1193). 

Toxic  Tremor  (alcohol,  opium,  nicotine,  mercury,     673 

etc.),  (658,  663,  780). 
Hysterical  or  Neurasthenic  Tremor  and  also  Trau-     674 

matic  Neuroses,  (1072-5). 
Paralytic    Dementia.      General    Paresis.      Paresis,     675 

(570,  763,  895,  1049,  1104,  1216,  1230). 

Lesion  of  the  Crus  Cerebri  or  Pons    involving  the    676 
Rubro-spinal  tract,  (441,  1270,  1325).    (Figs.  1S-20). 

Paralvsis  Agitans.     Parkinson's  Disease,  677 

(612,  766,  S00). 


Senile  Tremor.  67S 

Spasmus  Nutans.     Nictitatio  Spastica,  (690).  679 


les,  caused  by  cold  (physiological)  or  infection  (pathological)  and  resulting  in  an  increase  in  the  body's  temperature  and  may  be  followed  by  high  fever. 

coholism  in  ancestors,  etc.).     May  be  local  or  general.     Usually  in  advanced  age. 

ital  or  acquired,  in  early  childhood.     Often  associated  with  blepharospasm  and  oscillation  of  head. 

Usually  associated  with  photophobia. 

light  and  looking  sideways  constantly  while  at  work. 

'ertigo  associated  with  deafness  and  tinnitus  aurium  and  due  to  disease  of  inner  ear.      Nystagmus  in  the  opposite  direction  from  the  labyrinth  involved  occurs  occasionally  when  head  is  rotated 
id,  or  ear  syringed,  or  labyrinth  in  any  way  irritated.     The  caloric  reaction  (79)  is  absent. 

a  and  other  symptoms  of  disease  of  the  cerebellum.     The  nystagmus  is  usually  towards  the  side  of  the  lesion. 

Strong  heredity.     Knee-jerks  absent,  except  in  early  stage.    Babinski  is  present.     Optic  atrophy  rare.     Muscular  weakness  and  contractures  are  not  uncommon. 

i  heredity.     Intention  tremor.     Exaggerated  knee-jerk,  Babinski,  optic  atrophy  and  scanning  speech  are  common  symptoms.     Vertigo  is  usually  present  (932). 

d  in  local  lesions  (tumors  especially).     Nystagmus  is  commonly  present  in  bulbar  lesions,  especially  in  those  involving  the  cerebellar  peduncles  and  tracts  and  the  posterior  longitudinal  bundle. 

child's  head  is  held  still  and  the  tremor  prevented  (679).     Not  to  be  confounded  with  the  deep  bowing  (Salaam  cramp)  which  occurs  in  some  idiots  and  epileptics,  with  or  without  nystagmus.    Roll- 
occur  in  otitis  media  and  in  rickety  children. 

igmus  associated  with  jerking  movements  of  the  limbs  or  trunk,  aggravated  by  cold  and  by  percussion.    Associated  with  other  congenital  defects, 
liar  palsies  or  when  weakened  muscles  are  strongly  exerted. 

nesthesia  with  only  slight  anesthesia,  or  none  at  all.    Trophic  disturbances  and  mutilation.    Slight  tactile  impressions  are  often  painful. 

ibrillary  contraction  of  tongue  and  lips,  dysarthria,  dysphagia  and  spastic  paraplegia. 

ibrillary  contraction  of  small  muscles  of  hands  and  of  shoulder  girdle  combined  with  spastic  paraplegia. 

ibrillary  contraction  of  the  peronei  muscles.    Rarely  there  are  pain,  muscle  twitching  and  anesthesia. 

alaris  palpebrarum  but  may  occur  in  any  muscle.    It  consists  in  a  quivering  of  the  muscle  fibers  and  occurs  in  neurasthenic  and  exhausted  persons. 


6S2 

683 

6S4 

Labyrinthine     685 


Chills.     Rigors.     Shivering. 

Essential  Tremor. 

Amblyopia,  (359). 

Albinism. 

Miner's  Nystagmus. 

Menidre's    Disease.      Aural 
Vertigo,  (650,  918,  1019). 

Cerebellar  Disease,  (609-10,  648,  7S3,  1016,  1272).  686 

Friedreich's  Hereditary  Ataxia,  (670).  0S7 

Disseminated  Sclerosis,  (668,  765).  GS8 

Cerebral  Disease  (especially  of  the  brain  stem).  6S9 

Spasmus  Nutans.     Nictitatio  Spastica,  (679).  690 

Nystagmus-myoclonus.  691 

Ocular  Muscular  Insufficiency,  (810).     (Figs.  14,  IS).   092 

Syringomyelia,  (552,  S37-9, 1009, 1170, 1187, 1357-9).       693 

(Figs.  25-7.) 
Chronic  Bulbar  Paralysis,  (540,  1150).     (Fig.  21-2)       694 
Amvotrophic  Lateral  Sclerosis,  (547,  797,  1149).  695 

(Figs.  24-6.) 


Spinal  or  Neuritic  Muscular  Atrophy,  (496). 
Myokymia.     Myoclonia,  (293). 


696 
097 


CHART  XII  c 

Local  Palsies 

Comprising  Numbers  700  to  721  on  right  margin 

ite) — The  anesthesia  accompanying  these  palsies  can  be  seen  from  the  areas  of  cutaneous 
distribution  of  these  nerves  depicted  in  the  plates  at  the  end  of  the  book  (Figs.  33-8).    In  mild 

lesions  of  the  nerves  anesthesia  is  either  absent  or  much  less  marked  and  less  extensive  than 
the  motor  parah 


117 


Inability  to 
Move,  More 
or  Less, 
Muscles  of 


J 
A 
W 


DIAGNOSTIC  ANALYSIS  OF  SYMPTOMS 

LOCAL  PALSIES 

Abstract  of  Symptoms 
There  are  ptosis  and  strabismus  divergens  and  the  pupil  is  dilated 
and  immobile  both  to  light  and  accommodation  (this  condition  of 
the  pupil  may  occur  as  an  isolated  paralysis, — 333).  The  eye- 
ball can  be  moved  in  no  direction  except  outward  (abducens),and 
outward  and  downward  with  rotation  of  eyeball  (superior  ob- 
lique). For  symptoms  characteristic  of  the  isolated  paralysis  of 
each  ocular  muscle  see  Chart  XIV  c,  816.  When  the  superior 
oblique  muscle  is  paralysed  the  levator  palpebrae  superioris  is 
paralysed  with  it  and  ptosis  results. 
^  The  ocular  muscles,  except  the  levator  palpebrae  superioris,  have 
a  bilateral  cortical  representation.  Hence  ocular  paralyses, 
except  ptosis,  almost  never  occur  in  lesions  above  the  oculo- 
motor nucleus,  except  in  bilateral  lesions.  The  cortical  repre- 
sentation of  the  ocular  muscles  seems  to  be  very  diffuse  or 
multiple.  Conjugate  deviation  may  result  from  supra-nuclear 
lesions. 

For  the  symptoms  of  paralysis  of  the  trochlearis  (patheticus) 
nerve  and  of  the  abducens  nerve,  each  of  which  produces  a 
strabismus  convergens,  see  816. 

The  muscles  of  mastication  of  one  side,  rarely  of  both  sides,  are 
paralysed  and  in  severe  cases  atrophied.  The  temporal  and 
masseter  muscles  cannot  be  felt  firmly  contracting  when  efforts 
are  made  to  chew.  The  jaw  cannot  be  closed  tightly  or 
opened  strongly  or  moved  laterally  towards  the  healthy  side 
(external  pterygoids),  or  the  chin  pushed  forwards  (internal 
pterygoids).  Mastication  of  food  is  difficult  or  impossible; 
dysmasesis  (286).  The  jaw  reflex  (322)  is  abolished.  In 
some  cases  one  side  of  the  soft  palate  (tensor  veli  palatini) 
is  paralysed  and  in  some  the  hearing  of  low  tones  is  unpleasant 
■f      (tensor  tympani). 

In  trigeminus  lesions  there  is  unilateral  abolition  of  the  con- 
junctival, corneal,  sneezing  and  palatal  reflexes;  and  the 
secretion  of  tears  is  at  times  affected.  There  is  no  irritation,  or 
tears,  from  inhaling  ammonia  or  acetic  acid.  There  is  also  loss 
of  sense  of  taste,  and  dilatation  of  the  pupil,  narrowing  of  the 
eyelid  slit,  even  enophthalmus,  are  present.  Heat  and  redness 
of  skin  in  recent  cases  and  coldness  and  cyanosis  of  skin  in  old 
cases.  The  salivary  secretion  and  taste  are  affected  when  either 
the  proximal  or  the  distal  end,  but  not  the  middle,  of  the  nerve 
is  affected. 

The  muscles  of  expression  of  one  side  (rarely  of  both  sides)  of  the 
face  are  paralysed.  The  forehead  cannot  be  wrinkled  and  the 
eye  appears  larger  than  normal  and  cannot  be  closed  (lagoph- 
thalmus,  hare's  eye).  When  attempts  are  made  to  close  the 
eyelids  the  eyeball  turns  upward,  the  cornea  disappearing  behind 
the  upper  lid  (Bell's  phenomenon).  The  angle  of  the  mouth  is 
lower  than  normal  and  cannot  be  raised.  The  naso-labial  fold  is 
obliterated.  The  lips  cannot  be  firmly  closed;  so  that  whistling 
is  impossible  and  speech  is  impaired.  Mastication  is  difficult  be- 
cause the  weakened  buccinator  muscle  allows  food  to  collect  be- 
tween the  jaws  and  the  cheek.  The  platysma  is  also  paralysed; 
so  that  the  angle  of  the  mouth  cannot  be  drawn  downwards. 
Tears  may  flow  from  the  eye  and  irritate  the  cheek  and  saliva 
from  the  angle  of  the  mouth.  The  conjunctiva  may  become  in- 
flamed and  the  cornea  ulcerated,  because  the  eyelid  cannot  wink 
and  keep  the  conjunctiva  clean.  In  some  cases  the  facial  paral- 
ysis may  be  preceded  and  accompanied  by  pain.  In  severe  cases 
the  paralysed  muscles  exhibit  the  electrical  reaction  of  degen- 

148 


Diagnosis 
Paralysis  700 
of  Motor 
Oculi. 
(Figs.  14,  18). 


Paralysis  701 
of  Troch- 
learis and 
of  Abducens. 

Paralysis  702 
of  motor     ) 
branch  of  $ 
Trigeminus. 


Facial        703 

Paralysis. 

Bell's 

palsy. 

Prosopo- 

plegia. 

Facial 

Monoplegia. 

Facial 

Diplegia, 

(751,  928, 

1317). 


Inability  to 
Move,  Moee 
or  Less, 
Muscles  of 

THE 

F 
A 
C 

E 


LOCAL  PALSIES  (Continued) 

Abstract  of  Symptoms  Diagnosis 

eration.  Hearing  and  taste  are  frequently  impaired  and  disor- 
dered. When  taste  is  affected  the  salivary  secretion  is  also 
affected  In  the  earlystages  of  the  disease  the  face  isdrawnover 
toward  the  healthy  side  by  the  unantagonized  healthy  muscles. 
In  the  later  stages  the  face  may  be  drawn  back  again  perma- 
nently towards  the  paralyzed  side  by  the  contracting  newly 
formed  connective  tissue  in  the  degenerated  muscles.  Also  in 
the  early  stage  of  recovery  the  face  may  be  drawn  towards 
the  paralyzed  side  by  over-innervation  of  the  muscles  form- 
erly paralyzed,  and  may  exhibit  temporary  contractures  and 
spasms,  possibly  "associated  movements."  These  spastic 
symptoms  may  be  due  to  irregular  regeneration  of  the 
nerve.  The  upper  fibres  of  the  facial  nerve  have  a  bilateral 
cortical  representation  as  do  the  laryngeal  nerves.  Hence 
lesions  of  the  cerebral  hemispheres  paralyse  mainly  the  lower 
branch  of  the  facial;  the  eye  on  the  paralysed  side  can  be  closed 
but  is  easily  forced  open.  For  the  localization  of  the  differ- 
ent forms  of  facial  paralysis,  see  1317. 

Paralysis  of  the  pneumogastric  nerve  is  discussed  under  760.    In     Pneumo-  704 
addition  to  the  laryngeal  paralysis  there  is  often  present    dis-     gastric 
order  of  the  respiratory  act  and  of  the  heart  beat  (tachycardia).     Paralysis 

(760). 

When  the  tip  of  the  shoulder  sinks  downwards  and  forwards  and     Paralysis  705 
the  arm  cannot  be  easily  raised,  there  may  be  a  paresis  of  the    of  the 
trapezoid  muscle.    When  this  muscle  is  paralysed  on  both  sides,     Spinal 
the  head  tends  to  fall  forward.   When  the  head  is  drawn  towards     Accessory, 
one  shoulder  and  the  chin  turned  upwards  and  towards  the  other, 
the    sterno-cleido-mastoid    muscle   is   paralysed   on   that   side 
■{      toward  which  the  chin  turns.   This  posture  is  called  caput  obsti- 
pum  spasticum,  when  the  muscle  is  atrophied  and  secondarily 
contracted  and  the  deformity  can  no  longer  be  corrected  by 
passive  motion.    Caput  obstipum  spasticum  occurs  also  and  is 
more  pronounced  in  torticollis  from  spasm  of  the  muscle  (730). 
When  the  sterno-cleido-mastoid  muscle  is  paralysed  on  both 
sides,  the  head  tends  to  fall  backwards. 

The  tongue  when  protruded   (urns  towards  the  paralysed  side.  Hypo-       706 

When  both  sides  are  paralysed  the  tongue  cannot  be  protruded  glossus 

at  all,  and  in  such  cases,  apeech,  mastication  and  deglutition  are  Paralysis. 

difficult  and  imperfect.      In  lesions  of  the  nucleus  of  the  hypo-  (546,752). 
glossus  nerve  there  is   also  B  mild   paresis  of  the  orbicularis  oris 

muscle.  Intracranial  lesions  involving  the  hypoglossals  and 
other  nerve  roots  at  the  base  of  the  brain  may  cause  Avelli's 
syndrome:    pharyngo-laryngeal  or    glosBO-phaxyngo-laryngeal 

paralysis  (old);  or  may  cause  Schmidt's  syndrome:  the  above 
and  also  sterno-cleido-mastoid  and  trapezius   paralysis. 

phragm  is  paralysed  on  one  or  lioth  sides,  causing  dyspnoea     Phrenic     707 
on  exertion  and  unking  in  of  the  epigastrium  on  inspiration,     1'aralysis. 
■  iallv  on  deep  Inspiration.    The  lower  part  of  the  lung  a 

drawn  upwards  and  atelectasis  and  pneumonia  may  air.  He- 
sides  the  usual  o  and  neuritis,  tins  paralysis 
may  also  occur  in  pleurisy,  peritonitis,  trichinosis  and  in  bulbar 

and   spinal    lesions.      The    paralysed   diaphragm   shows    l.ittt 

phenomenon. 

The  supra-.'tnd  infra  spmatus  musclefi  are  paralysed:  BO  thai   rota-  Supra-        708 

tion  of  the  arm  out  ward  and  rai^iiu;  it  in  abduction  are  impaired.  Scapular 

Muscles  involved  are  atrophic  and  ulnar  side  of  hand  is  turned  I'arah 
forwards. 

Thcserratus  anticus  major  [a  paralysed:  BO  that   when  the  scapula      Long  TOfl 

is  raised,  its  lower  angle  approaches  the  vertebrae  and  the  inner    Thoracic 
margin  of  the  scapula  does  nol  !"■  do  e  to  the  thorai  and.  on    Paralysis, 
movements  of  the  arm  upwards  and  forwa  from  the    Berratus 

thorax  like  a  (ring.      The  arm  cannot   lie  raised   heyond  a  hori-      Paralysis. 
■Ontal   line. 

1 19 


Inability  to 
Move,  More 
or  Less, 
Muscles  of 
the 


LOCAL  PALSIES   (Continued) 
Abstract  of  Symptoms 
Motion  of  the  arm  inward  and  forward  is  impaired. 
Hand  cannot  be  placed  on  opposite  shoulder. 


Diagnosis 
Anterior  and  Posterior  710 
Thoracic  Paralysis. 


Rotation  of  the  arm  inward  and  motion  of  the  arm  backward 
are  impaired. 


Sub-Scapular  711 
Paralysis. 


The  deltoid  and  teres  minor  are  paralysed:  so  that  the  arm  can- 
not be  raised. 

The  combined  paralyses  of  the  brachial  plexus:  Erb's  and  Klump- 
ke's  paralysis,  are  discussed  under  454,  455  and  490. 


Axillary     712 
Paralysis. 


The  biceps,  brachialis  anticus  and  coraco-brachialis  muscles    are     Musculo-  713 
more  or  less  completely  paralysed;  so  that  flexion  of  the  arm  at     Cutaneous 
elbow  is  more  or  less  impaired,  especially  in  supination  (very  rare).     Paralysis. 


The  pronators  and  flexors  of  the  hands  and  fingers,  the  muscles  of 
the  ball  of  the  thumb  and  the  first  and  second  lumbrical  muscles 
are  paralysed.  The  hand  can  neither  be  flexed  nor  pronated. 
The  thumb  cannot  be  brought  across  hand  to  touch  the  little 
finger,  but  remains  close  to  the  index  finger  (ape's  hand).  The 
first  (proximal)  phalanges  of  fingers  can  be  flexed,  but  not  the 
second  and  third  phalanges. 

The  interossei,  the  third  and  fourth  lumbricals,  and  the  muscles 
of  the  little  finger  are  paralysed.  The  proximal  phalanges  can- 
not be  flexed,  the  other  phalanges  cannot  be  extended  and  the 
little  finger  cannot  be  moved.  The  fingers  cannot  be  spread. 
When  muscle  atrophy  and  contracture  occur  "claw  hand"  results. 

The  extensors  and  supinators  of  the  hand  and  fingers,  and  the  ab- 
ductor pollicis  longus,  are  paralysed.  The  thumb  is  adducted  and 
can  neither  be  abducted  nor  extended.  Wrist-drop  and  slight 
pronation.  Wrist  and  fingers  cannot  be  extended  completely. 
The  wrist-drop  differs  from  that  of  lead  palsy  (494)  in  that  the 
supinator  longus  is  paralysed.  Therefore,  if  the  forearm  is  held 
midway  between  supination  and  pronation  and  the  elbow 
strongly  flexed  against  a  resistance  offered,  the  belly  of  the 
supinator  longus  will  not  stand  out  firmly  contracted  as  it  will 
in  lead  paralysis  and  in  health. 

The  extensor  femoris  is  paralysed;  so  that  flexion  of  the  thigh 
on  the  body  and  extension  of  leg  on  thigh  are  impossible  or 
difficult.  Standing  and  walking  are  difficult,  and  ascension, 
jumping  and  running  impossible. 

The  adductor  muscles  of  thigh  are  paralysed;  so  that  adduction 
of  leg,  pressing  of  thighs  together  and  crossing  of  legs  are  im- 
possible. 

The  glutei  muscles  are  paralysed;  so  that  walking,  ascending 
stairs,  straightening  up  of  body,  abduction  and  rotation  of 
thigh  are  impaired.     Generally  much  muscular  atrophy. 

Foot  and  toes  are  paralysed ;  the  leg  cannot  be  flexed  on  thigh  and 
rotation  of  the  thigh  is  impaired.  In  cases  of  isolated  tibialis 
paralysis  there  is  absence  of  plantar  flexion  of  foot,  and  of 
plantar,  flexion,  spreading  and  adduction  of  toes  (Pes  calcaneus 
et  valgus).  In  cases  of  isolated  peroneal  paralysis  there  is 
absence  of  dorsal  flexion  and  abduction  of  foot  and  its  adduc- 
tion impaired — absence  of  dorsal  flexion  of  toes.  There  are  foot- 
drop,  high  stepping  gait  and  Pes  equino-varus. 

For  paralysis  from  lesions  of  the  cauda-equina,  see  487, 1007  and 
1308. 

150 


Median      714 
Paralysis. 


Ulnar        715 
Paralysis. 


Musculo-  716 
Spiral  and 
Radial 
Paralysis. 


Crural        717 

Paralysis 

(997). 


Obturator  718 
Paralysis. 


Gluteal      719 
Paralysis. 


Sciatic       720 
Paralysis. 
(996) 


Cauda 
Equina 
Paralysis* 
(Fig.  29). 


721 


CHART  XII  d 

Local  Spasms 

Comprising  Numbers  725  to  733  on  right  margin 


l.M 


DIAGNOSTIC  ANALYSIS  OF  SYMPTOMS 
LOCAL  SPASMS 

Abstract  of  Symptoms 
The  jaws  are  held  tightly  shut  and  the  masseter  and  temporal  mus- 
cles can  be  felt  to  be  contracted  (lock  jaw),  usually  bilaterally. 
The  spasm  may  be  "tonic,"  as  in  tetanus  (606),  tetany  (614),  irri- 
tation of  teeth  (wisdom  teeth)  and  certain  unilateral  lesions  of 
the  pons  and  medulla;  or  "clonic,"  as  in  chills  and  in  rare  cases  of 
paralysis  agitans  and  hysteria.  When  the  pterygoid  muscles  alone 
are  in  spasm  the  mouth  is  held  open  and  cannot  be  closed. 

'  Spasms  of  one  or  more  muscles  of  expression  of  the  face,  unilateral 
or  bilateral,  are  relatively  common,  as  in  convulsive  tic  (601) 
and  tic  douloureux  (602).  These  spasms  are  often  a  mixture  of 
tonic  and  clonic  contractions,  the  clonic  predominating.  They 
may  affect  all  the  muscles  or  only  one,  as  in  tonic  spasm  of  the 
orbicularis  palpebrarum  (blepharospasm)  (601,  617),  or  in  clonic 
spasm  of  this  muscle  (spasmus  nictitans:  nictation).  The  platysma 
myoides  often  takes  part  in  these  spasms  and  very  rarely  the 
muscles  of  the  soft  palate  and  the  internal  and  external  ear  mus- 
cles. Very  rarely  spasm  of  some  of  the  facial  muscles  about  the 
mouth  constitute  an  occupation  neurosis  or  cramp,  as  in  the 
"Auctioneer's  cramp"  and  "Cornet  player's  cramp."  These 
facial  cramps  may  be  symptomatic  directly  of  lesions  of  the  cort- 
ical facial  center,  of  the  facial  nerve  in  its  course,  and  reflexly  of 
the  trigeminal  nerve  or  its  terminal  filaments  in  the  eye,  nose, 
mouth  or  ear.  There  is  also  to  be  remembered  the  passive  con- 
tracture of  the  degenerated  muscles  and  the  active  contracture 
due  to  over-innervation  of  the  convalescing  muscles  in  facial  paral- 
ysis. Causeless  and  uncontrollable  laughter  must  also  be  classed 
among  the  facial  spasms.  This  condition,  similar  to  the  allied 
state  of  causeless  and  uncontrollable  crying,  occurs  especially  in 
hysteria  and  in  lesions  of  the  optic  thalamus. 

'  Spasm  of  the  pharynx  of  a  tonic  nature  preventing  swallowing  and 
of  a  clonic  nature  repeating  the  act  of  swallowing  with  great  fre- 
quency occur.  The  former  occurs  in  hydrophobia  (607)  and  some- 
what also  in  tetanus  (606) ;  while  the  latter,  associated  with  coma, 
frequently  occurs  in  mild  epileptic  attacks.  The  spasm  also  occurs 
from  irritation  of  the  pharynx  in  hysteria  and  very  rarely,  as  one 
of  the  crises  in  locomotor  ataxia  (433).  Spasm  of  the  oesophagus 
is  not  uncommon  in  hysterical  persons  and  makes  the  swallowing 
of  food  very  difficult. 

Spasm  of  the  muscles  of  the  larynx  (spasmus  glottidis,  false  croup, 
laryngismus  stridulus),  causing  noisy  and  difficult  breathing,  is  a 
not  uncommon  and  occasionally  a  dangerous  condition.  It  occurs 
almost  exclusively  in  children  and  is  often  associated  with  rickets 
and  with  digestive  disorders.  Occurs  also  in  general  diseases  such 
as  hydrophobia,  hysteria,  epilepsy,  chorea,  tabetic  crises,  etc. 
Sneezing  (sternutatio  spastica,  ptarmus)  and  coughing,  reflex  acts 
implicating  both  the  pneumogastric  and  the  intercostal  nerves, 
are  often  due  to  pathological  conditions  and  irritation  of  the 
nervous  system.  Bradycardia,  Cheyne-Stokes'  respiration  and 
cerebral  vomiting  are  symptoms  of  irritation  of  the  pneumo- 
gastric nucleus,  but  are  not  characteristic  and  are  of  little  diag- 
nostic value. 

r  Spasm  of  the  tongue  is  very  rare,  especially  so  the  tonic  form.  Dur- 
ing the  attack  speaking  and  swallowing  is  impossible.  Very  rarely 
a  tonic  spasm  of  the  tongue  occurs  when  the  patient  attempts  to 
speak  (stuttering  and  aphthongia).  Spasm  of  the  tongue  is  some- 
times associated  with  facial  spasm  and  with  spasm  of  the  sub- 
maxillary muscles.  These  spasms  may  be  due  directly  to  lesions 
of  the  cortical  tongue  center,  of  the  hypoglossus  nerve  in  its  course, 
or  reflexly,  especially  from  lesions  of  teeth,  mouth  and  nose. 

152 


Diagnosis 
Trige-        725 
minal 
Spasm  or 
Cramp. 
Trismus. 


Facial        726 
Spasm  or 
Cramp 
(267,  601). 


Glosso-      727 
Pharyn- 
geal 

Spasm  or 
Cramp. 


Pneumo- 
gastric 
Spasm 
or  Cramp. 


72S 


Hypo- 
glossus 
Spasm  or 
Cramp. 


729 


Spasm  of 
Muscles  of 


I) 
I 
A 
P 
II 
R 
A 
G 
M 


A 
B 

I) 
0 
M 
E 
N 


LOCAL  SPASMS     (Continued) 

Abstract  of  Symptoms 

Spasm  of  the  neck  muscles,  especially  the  sterno-cleido-mastoid : 
caput  obstipum  (spastic  wry  neck),  is  sometimes  congenital  and 
is  sometimes  acquired  in  later  life.  In  these  cases  the  head  is 
drawn  toward  the  shoulder  of  the  affected  side  and  the  chin  is 
turned  toward  the  other  side  and  slightly  elevated  and  the 
sterno-cleido-mastoid  muscle  can  be  felt  to  be  firmly  contracted. 
When  the  trapezius  is  the  seat  of  the  spasm  the  occiput  is  drawn 
backwards  and  turned  toward  the  shoulder  of  the  affected  side 
and  the  edge  of  the  muscle  can  be  felt  to  be  firmly  contracted. 
Spasm  of  the  muscles  is  sometimes  tonic,  sometimes  clonic  and 
often  both.  The  cause  of  these  spasms  is  often  neurotic  and 
often  rheumatic.  Rarely  it  is  some  disease  of  the  eye  or  of  the 
ear  (torticollis  ab  oculo  laeso,  ab  aure  laesa)  or  of  the  cervical 
vertebrae.  Usually  many  muscles  are  involved,  although  one  or 
two  more  prominently  than  the  others. 

Tonic  spasm  of  the  diaphragm,  either  unilateral  or  bilateral,  occurs 
very  rarely  and  produces  dangerous  dyspnoea.  It  sometimes 
occurs  as  one  symptom  of  a  general  disease :  tetanus,  hydrophobia, 
hysteria,  etc.  Clonic  contractions  are  common  and  cause  hic- 
cough (singultus),  always  a  distressing  and  at  times  a  dangerous 
symptom,  which  occurs  occasionally  in  brain  and  spinal  cord 
lesions  and  frequently  in  irritation  of  the  pneumogastric  nerve, 
especially  from  the  gastric  mucous  membrane.  A  similar  but 
slower  contraction  of  the  diaphragm  associated  with  facial  spasm 
(opening  of  mouth)  causes  the  act  of  yawning  (oscedo,  chasmus) 
which  is  sometimes  frequently  repeated  as  an  aura  of  apoplexy  or 
epilepsy  and  occurs  also  in  hysteria,  digestive  disorders,  drowsi- 
ness, etc. 


("Tonic  and  clonic  contractions  of  some  or  all  of  the  abdominal  mus- 
■l     cles  occur  with  extreme  rarity,  and  are  usually,  if  not  always, 
hysterical. 


Diagnosis 

Spinal       730 
Accessory 
Spasm  or 
Cramp 
(601). 


Phrenic 
Spasm  or 
Cramp. 


rai 


Inter 

costal 

Spasm. 

Abdominal 

Spasm. 


732 


A 

i; 

M 

\ 

N 
D 

I. 
I 

<; 


Tonic  and  clonic  spasms  of  the  muscles  of  the  arm  and  shoulder  Brachial,  738 

or  of  the  leg,  with  the  exception  of  the  secondary  contractures  or  Lumbar, 

due  to  lesions  of  the  pyramidal  tract  and  of  the  peripheral  nerves,  or  Saiatio 

arc    very    rare      They    usually    are    due    either    I"    deficiency    of  Plexus, 

water  in  the  system,  and  often  occur  in  disease  in  which  much  Spasm  or 

water  is  lost,  as  cholera,  diarrhoea,  etc,  or  to  hysteria,  or  to  Cramp 
rheumatic   factors,   or  are   reflex.     The   deformity   resulting  in 
each  case  can  be  predicted  from  the  function  of  the  muscle 
involved. 


153 


CHART  XIII 

Disorders  of  Speech  and  Gait 


Symptoms 
Analysed 


735 

DISORDERS 

OF  SPEECH, 

READING 

AND 

WRITING. 


736 
DISORDERS 

OF  GAIT. 


DIAGNOSTIC  ANALYSIS  OF  SYMPTOMS 
Character  of  Disorder 


737 

ANARTHRIA  (283) 

Inability  or  unwillingness  to  speak.  No 
disease  of  vocal  organs  or  peripheral 
nerves.  This  condition  may  result  from 
a  complete  aphonia  (260)  or  complete 
aphasia  (221)  or  complete  dysarthria 
(284). 


The  diseases  in  which  Anarthria 
and  Dysarthria  occur  are  set 
forth  in  Chart  XIII  a. 


73£ 

DYSARTHRIA  (284) 
Ability  to  express  thought  by  speech  but 
articulation  is  defective. 

739 

APHASIA  (221) 

Articulation  normal  but  expression  of  nor- 
mal thought  is  defective. 


740 
ATAXIC 

741 

PARALYTIC  AND  FLACCID 


742 

I'M:  A  LYTIC  AND  SPASTIC 


The  varieties  of  Aphasia  and  the 
conditions  under  which  they 
occur  are  set  forth  in 
Chart  XIII  b. 


Tin'  dfaeBBM  in  which  Disorders 
of  Gail  occur  arc  set  forth  in 
Chart  XIII  o. 


I :.: 


CHART  XIII  a 
Anarthria  and  Dysarthria 

Comprising  Numbers  737  and  738  on  left  side  of  Chart 
and  743  to  768  on  right  margin 


157 


737 

■Result  "t"  ■  ! 

A 

infancy,  or  congen- 

.\ 

ital. 

A 

R 

'I'      -i, 

II 

i; 

A 

Result  of  disease  in 

'"adult  life. 

DIAGNOSTIC  SI  MPTOMS  AM)  TESTS 

Auditory     memorii  ng    |  May  make  noises  bul  i 

spoki'ii    v.i  !  .(■!•  acquired,  or  were  earrj 

lost  through  disease;    hence   innervation    memories    ■ 


i    were   never  learned. 


Innervation  mi  ssary  for  spcccli  ha 

acquired  but  are  no)  available.    No  hysterical  symp 
toms. 


Can  be  t  r:t i hoi  1  to  speak  through  tl 
Bight. 

Complete  absence  of  speech,  and  ren 
is    impossible.      Patient    i 
speak  hi-  in  communicate  by  gestui 


'Congenital. 


Defective 

Education. 


738 
D 
Y 
S 
A 
R 
T 
II 
R 
I 

A 

284, 
188 


Paralytic. 


Hysterical    symptoms    and    etiological 
although  nut  always  prominent. 


Apoplectic  symptoms  (504  I, 

I  Vocal  organs  defective. 
normal. 
Vocal  organs  normal. 


The  labials,  the  Un- 
guals nr  i  hi-  vowel 
sounds  or  all  nf 
them  cannot  be 
properly  pronounc- 
ed. A  careful  ex- 
■  i  ion  reveals  a 
paralysis  i.r  a 
sis  within  the  do- 
main of  the  facial, 
the  hypoglossal  or 
the  pneumog 
nerve. 


No    symptoms    of 

any  central  disease. 


Will  neit  her  «  hisper  nor  speak. 
I  Can  whisper  faintly  but  distinctly. 
May  iniitti  r  but  cannot  artioi 

Words  imperfectly  formed,  also  a  nasal  voice.      An 

Words  imperfecta   formed  and  usually  a  very  limib 

Substitution  of  one  letter  for  another.     An  examinai 
speaks   the  vowels  correctly  but  has  difficul 

'Patient  cannot  whist  le  or  close  lips  tightly, 

Tongue  is  not  protruded  straight  but  devi 

Soft   palate  is  not  raised  (bilateral)  or  not  raise 

Anesthesia  of  larynx.     Paralysis  of  crico-thjm 
on  lower  level)  and  of  thyreo-ary-epiglottis 


Immobility  of  one  or  both  vocal  cords  from  par 
vcrie  position  of  cords  (between  extreme  addi 

in  cases  of  unilateral   paralysis,  the    healthy    cord    n 
paralysed  cord. 


Immobility  of  one  or  both  vocal  cords  from  pal 
cord  or  cords  lie  near  the  median  line  (extra 
become  smaller  on  inspiration. 


Immobility  of  one  or  both    vocal    cords   from  pa 
arytenoid  lateralis  muscles)  and  in  some  CS  ■ 
and  hoarse.     Cords  are  wide  open  (abduction)  i 


May  be  symptoms      rjnj]ateraj  or  bilateral  paralysis  of  the  soft  palate,  ol 

l.ol    central    disease,  n   .i      ■  ,  ,  i  .l 

all  the  laryngeal  muscles  and  anesthesia  of  larynx 


Slow  and  clumsy  speech.  Cerebellar  gait. 


Speech  sounds  as  if  a  force 


Tremor  and  Ataxia.- 

Rigidity. 

Spasm. 


Tremulous  and  slovenly  spi 

ton !.   letters   and  syllables  are 

left  out  both  in  speaking  and  writing. 


!  Argyll-Robertson's  phenol 
Evident  mental  do-  I  attacks  may  occur  r 
terioration. 

[  Alcoholic  history,  appear 


ng  speech.  Intention  Tremor. 

M'.n  I'onous  speech.  Passive  Tremor. 


Great  variety  of  widespread 
Rigidity  of  muscles  and  slight  fli 


D  letters  (consonants)  are  spoken  with  difficulty  and  are  repeated  many  times  imperfectly  bi 

mce  is  arrested  by  a  spasm  of  one  or  more  of  the  muscles  concerned  in  speech,  such  as  the  hy] 
I        is  directed  to  the  speech  the  worse  it  becomes.     Singing  is  usually  not  at  all  affected. 


DIAGNOSTIC  ANALYSIS  OF  SYMPTOMS 

ABSTRACT  OF  SYMPTOMS 


Expressions  of  face  and  aclii 
of      Expressions  of  face  and  actii 


•  idiotic. 

;  normal. 


npossible. 
are   possible 


Patient  exhibits  little 


ntelligence  and  hi 


but  the  most  elementary  education,  if  of  any.     Soils  himself  with  urine  and  feces. 


Patient  shows  a  good  intelligence,  but  can  exp 
suit  of  careful  training.     Some   deaf  mutes 


loud    f  Absence  of  facial  expression  and  of   all  volu 
t  to    j      tary  actions. 

[  Facial  expression  and  actions  are  abnormal. 


.  a  deep  sleep  and  cannot  be  aroused  to  any  expression  of  consciousness 


Patient  is  evidently  insa 
usually  either  of  fear  i 


t  and  has  delusions.     When  recovery  has  taken  place  it  : 
of  a  divine  command  (delusional  insanity).    Anarthria  i 


itory  shows  that  he  never  had  any.     Incapable  of  any 


ess  himself  only  by  gestures  and  that  only  as  the  re- 
can  be  taught  to  speak,  generally  very  imperfectly. 

or  intelligence  by  stimulation  of  any  sensory  surface. 


ly  be  learned  that  his  silence  was  due  to 
ilso  common  in  profound  dementia. 


delu 


Hysterical  appearance.     Placid  and  contented. 


(Probably  only  a  severe  form  of  hysterical  aphonia.     It  is  a  rare  condition.     Most  cases 
Can,  by  hard  urging,  be  made  to  whisper  some  words  faintly  but  distinctly. 
ly.     Sudden  onset,  usually  followed  by  speedy  death.     Paralysis  of  motion  or  sensation  or  of  both  in  the  extremities, 
ation  of  the  vocal  organs  shows  no  paralysis,  but  a  developmental  defect;  such  as  cleft  palate  and  similar  malformations, 
abulary.     Intelligence  very  defective.     Paralyses,  usually  of  the  spastic  variety,  may  be  present  in  the  extremities. 


t  be  persuaded  to  whisper  a  few  n 


:  the  vocal  organs  shows 
ng    certain  consonants  e 


i  defects  or  paralysis.     Patients  exhibit  a  rather  childish  or  affected  form  of  speech.     Some  substitute  "W"  for  "R",  others  use  "TH"  for  "S",  etc.     In    idioglossia  a  child 
substitutes  others  for  them;   thus  apparently  invents  a  new  language.     This  speech  usually  becomes  normal  as  the  child  grows  older. 


;ide,  or  cannot  be  protruded  at  all. 


lly  (unilateral)  in  phonatii 


ical  cords  not  tense  in  phonation  and 
ottis  immobile). 


ost  all  the  laryngeal  muscles.  Cada- 
extreme  abduction).  In  phonation, 
icross  the  median  line  to  reach    the 


Labials  cannot  be  clearly  spoken,  especially  when  the  paralysis  is  bilateral. 

Li'nguals  cannot  be  clearly  spoken.     This  difficulty  is  usually  temporary.     Nasal  voice. 
Liquids  may  regurgitate  through  nose. 

Nasal  voice.     Indistinct  articulation,  which  is  improved  when  head  is  thrown  backwards. 

Voice  hoarse.  In  swallowing,  larynx  is  not  well  closed;  so  that  food  enters  it,  causing  cough, 
dyspnoea  and  possibly  deglutition  pneumonia. 


are  sucked  together  during  inspiration,  giving 
a  slight  stridor. 


Other  facial  muscles  are  paralysed. 

May  be  evidence  of    injury  or    pressure  upon  hypoglossus  nerve. 


May  follow  diphtheria. 
May  follow  diphtheria. 


4 

m 

1 1 

V  \ 

— v   -<. 

fill 

\-M\ 

p 

\\ 

\    \£ 

J/f 

& 

Liquids    may  regurgitate    through  nose. 


Tumor  or  lesion  along  course  of,  or 
in,  recurrent  laryngeal  nerve,  espe- 
cially lesions  of  the  aorta  or  lungs. 


Voice  very  little  altered.  If 
bilateral,  there  is  great 
inspiratory  dyspnoea  with 
stridor. 


ico-arytenoid  poslerior  muscle.     The 
in)  leaving   narrow   slit    which    may 


one  or  both  the  adductors  (thyro- 
Is  as  well.  Aphonia,  or  voice  is  weak 
part  of,  their  course.     Edges  concave. 


here  are  aphonia  or  hoarseness  and  nasal  speech  and  some  dysphagia.  There  may  be  respira- 
tory dyspnoea  and  deglutition  pneumonia.  If  both  nerves  are  slightly  affected  there 
may  be  rapid  and  irregular  cardiac  action  and  slow  and  irregular  respiration;  if  severely 
affected,  death  occurs. 

as  in  the  mouth  (hot  potato  speech)  and  frequently  chi 


May'be  a  tumor  or  lesion  along  the  recurrent  nerve.  May  be 
the  first  symptom  of  an  entire  recurrent  paralysis,  or  one 
symptom  of  a  more  general  disease  (bulbar  paralysis,  tabes, 
multiple  sclerosis,  etc.). 


Evidence  of  inflammation  of  the  larynx. 
History  of  over  use  of  the  voice. 


Hysterical  symptoms. 


of  pressure  upon  pneumogastrie  nerve. 


ulbar  symptoms  (434)  with  hemiplegia  or  paraplegia  and   exaggerated   tendon    reflexes. 
In   pseudo-bulbar  paralysis  (54G,  553)  the  speech  is  also  thick  and  indistinct. 


7).    History  of  syphilis.    Lumbar  puncture  shows  globulin  and  lymphocyt 
and  steadily  progressive  dementia.     Wassermann  usually  positive. 


pitch.    Symptoms  of  hereditary  ataxia. 

'atients  are  restless  and  especially  i 


ritable  and  violent,  although  usually  amiable      Apoplectiform  and  epileptiform 


r  and  breath.     Temporary  nature.     Foolish  pp3ech  and  actions. 

and  sensory  symptoms.     Nystagmus,  exaggerated  knee-jerk,  Babinski.     The  speech  is  jerky  and  somewhat  resembles  the  scanning  of  verse. 

3n  of  most  joints.     Attitude  is  that  of  bending  forward.     Mask-like  face.     Festinating  gait.     Speech  also  shows  festination  at  times. 

e  they  are  finally  uttered  explosively.     Speech  is  explosive  and  full  of  repetition  of  certain  sounds. 

lossus  (aphthongia).     There  is  difficulty  in  relaxing  the  muscle  spasm  so  that  words  can  be  uttered.     The  same  word  is  repeated  several  times  before  others  can  be  spoke 


Idiocy,  (1081). 

Deaf  Mutism. 

Coma,  (205,  1037). 
Insanity,  (1041). 

Hysterical  Mutism,  (1074). 

Hysterical  Aphonia,  (750,  107-1). 

Apoplexy  in  pons  or  medulla. 

Cleft  Palate,  etc. 

Imbecility,  (10SS). 

Lisping  and  Lalling  and  Idioglossia. 

Paralysis  of  Facial  nerve,  (703,  928,  1317). 
Paralysis  of  Hypoglossus  nerve,  (70G). 

Paralysis  of  Levator  Palati. 

Paralysis  of  Superior  Laryngeal  Nerve. 


Paralysis  of  the  entire  Recurrent  Laryngeal  Nerve 
(Reeurreos  Paralysis). 


Paralysis  of  Crico-Arytenoid  Posterior^Nerve 
(Abductor  or  Posticus  Paralysis). 


Hysterical  Aphonia,  (748). 

Paralysis  of  Pneumogastrie  Nerve  trunk,  (704). 
Bulbar  Paralysis,  (434,  544,  546,  694,  756,  1150). 

Friedreich's  Hereditary  Ataxia,  (652,  670,  687,  7S1). 
Paresis,  (134,  177,  579,  675,  895,  1049,  1104,  1216,  1230) 

Alcoholism,  (585,  65S,  663,673,  780,953,   1030,   1053,   1101, 

1107,  1109). 
Multiple  or  Disseminated  Sclerosis,  (511,  5S0,  659,  668,  6SS, 

756,  799,  913,  1051). 
Paralysis  Agitans,  (612,  677,  800). 

Stammering  (Anarthria  Literalis). 

Stuttering  (Anarthria  Spasmodica  or  articulative  tics). 


749a 
750 


CHART  XIII  b 
Amnesia  and  Aphasia 

( 'oni|>ri.sing  Numbers  7:W  on  left  side  of  ( iharl 
and  769  to  777  on  righl  margin 


1 59 


DIAGNOSTIC  A 


AMNESIA  AND  \PII.\H  \ 
221  to  227) 

None  "i  these  conditions 
constitutes  a  disease,  bu1 
is  rather  one  sj  mptom  of 
a   more    complex   disease. 

Each  is  a  form  of  de- 
mentia in  the  broad  sense 
of  the  term  and  consists 
in  a  loss  of  general  or 
i  memories.    See  also 

Vnarthria  and    Dysarthria 

7:;s-s 


Patient  is  capable  of  normal  speech  but  ex- 
hibits a  decided  Ins.-  of  memory. 


Patient  is  incapable  of  normal  speech  for 
want  of  innervation  memories  of  a  Few  or 
many  spoken  words. 


Patient  is   incapable  of   normal  speech   for 

want    of     auditory     memories  of    spoken 
words. 

Patient     is   incapable    of   normal  speech   for 

want     of    visual    memories    of  written    or 
printed  words. 


AMNESIA,  ; 

U'.sti; 

I  he  loss  of  memory  may  not  be  accompanied  by  any,  i 

of  the  names  of  persons  is  rather  common  ami  of  no 

or  less  distant  past,  are  referred  by  the  memory  to  I 

cerebral  concussion  and  compression  (1042-3 

!       little  time  immediately  previous  to  the  injiin    and   Eri 

I  Examination  of  the  patient  shows  a  loss  of  mei 

in  old  people  and  ill  the  insane,  and  i-  usual] 

Can  express  ideas  by  gestures,  but  cannot  name  object 
when  it  is  spoken  to  him  and  can  often  then  pronou 
one  or  two  weirds,  or  even  to  none  (anarthria).     I  sei 
and  often  even  when  it  is  not.    ( 'anno!  const  rui 
s- i 1 1 ii  songs.    When  his  arm  is  not  paralysed  patient 

Can  usually   read  but    not   aloud.      The  condition   is  u 

Patient    Tails  to  understand   more  or  leSS  of  w  li.it    is  said 

what    he    repeats.      Cannot   execute  Verbal  CO] and-. 

COnSCioUS  of  this  mistake  even  when  bis  attention   i-   i 

Patient  cannot  name  objects  seen,  or  read  written  01  p 
('annot  execute  written  commands,  lint  readih  I  MCU 
Can   write  from  dictation  imperfectly,  lint    noi   at   all 


AGHAPill  \ 


Patient   is  incapable  of  normal  speech   from   loss  of  innervation   memories  and   of  auditory        Patient 
memories  of  spoken  words.  ,i       I, 

called 

Patient   is  incapable  of  normal  speech  from  loss  of  proper  associations  and  of  appreciation  of       Patient 
I     the  memories  concerned  in  speech.  exhibi 

I  Patient  is  incapable  of  writing  for  want    of   the  B< 
Patient  B  Bpeech   is   normal,   but  his  writing  is  abnormal.    J      condition  uncomplicated  by  tor  aphasia. 

(.Patient  omits  words  in  writing,  usee  the  wrong  words,  i 


Broca,  in  1861,  published  a  case  of  motor  aphasia  with  a  lesion  at  the  base  of  the  left  inferior  frontal  convolution  and  thereby  laid  I 

Wernicke   whose  Btudies  have  contributed  greatrj  to  the  comprehension  of  aphasia)  divided  motor  and  sensory  aphasia  into  threi 

l-t.    Cortical  Motor  Aphasia,  in  which  the  patient  i-  unable  to  speak,  write  or  read  aloud  correctly,  or  to  speak  or  writ 

2nd.     Sub-cortical  Aphasia,  in  which  the  patient  can  neither  speak  spontaneously  nor  from  dictation  nor  read  aloud  co 

3rd.    Transcortical  Motor  Aphasia,  in  which  the  patient  can  neither  speak  nor  write  correctly,  but  can  speak  and  write  iron 

1st.    Cortical  Sensory  Aphasia,  in  winch  the  patient  can  speak  (with  paraphasia)  and  copy,  but  can  neither  m 

2nd,     Sub-cortical  Sensor}  Aphasia,  in  which  the  patient  can  speak  quite  perfectly,  write,  copy,  read  aloud  and  undei 

3rd,    Transcortical  Sensor)  Aphasia,  in  which  the  patient  can  speak  (with  paraphasia)  and  write  (with  paragraphia)   i  m  cop 

Wernicke  also  recognizee  a  Conduction   Aphasia,  in  which  the  patient  can  -peak,  write  and  read  and  understand  correctly,  bu 

Mane  considers  all  form-  iii  aphasia  as  resulting  from  a  greater  or  less  degree  of  a  general  intellectual  impairment  rather  than 
phasia  with  difficulty  of  articulation  dysarthria).     Whether  he  is  altogether  right  in  this  or  not,  certainly  our  concept - 


ipn.i-ia  with  difficulty  ni  articulation  (anarthria oi 
neither  of  which  i-  probably  altogethei  falsi 


LYSIS  OF  SYMPTOMS 


1ASIA  AND  AGRAPHIA 

T  OF  SYMPTOM- 

ill--  by  very  little,  intellectual  impairment  in  other  resp  I      .  in  degree  the  loss  of  memory 

or  prognostic  value.     "Retroacti  ;     iccurred  in  thi 

mmediati   past,  as  in  Korsakoff's  psychosis  (1100  unnesia"  occurs  in  some  i 

ted  with  fright.     In  it,  memory  is  losl  of  those  events  which  occurred  during 

iaQv  for  recent  events,  imp  leral  failure  of  mental  powers.     Very  common 

1  wiili  mental  depression. 

•II   oral  all.    Can  use  verbs  better  than  nouns  and  proper  names.     Recognizee  the  desired  word 

it      In  speaking,  the  patienl  is  frequently  at  a  loss  for  a  word.     His  vocabulary  is  limited  often  to 

paraphasia     775)  but  is  often  conscious  of  his  mistake  if  his  attention  is  called  to  it 

.    agrammatisrnus),  bul  canoften  repeal  sequences  of  numbers,  days,  months,  etc.,  and  can 

write  from  ropy,  but   makes  many  mistakes  in  spontaneous  writing  (paragraphia 

t>-i|  with  right-sided  hemiplegia  in  right-handed  persons  and  vice-versa. 

J  "" epeat  what  i-  said  to  him,  or  if  in  rare  cases  he  can  do  this,  he  dor-  not  understand 

ittcn  ones      In  speaking,  the  patienl  frequently  uses  a  wrong  word  and  is  not 
d  I.,  n     <  an  write  spontaneously  and  from  copy  but  not  from  dictation.     He  ran  read  well. 

■'d-.  but   may  at  times  recognize  and  name  objects  which    hi     touches    and    feels, 
H-rl.al  ones      In  speaking,  patients  rare  conscious  of  their  mistakes 

a  copy  and  make  man)   mistakes  in  spontaneous  writing.    Cannot  read  what  they  have  writ! 

nam.-  objects  nor  understand   words  spoken   to  him.     In   speaking,  patient    is  frequently 
wrong   one  and  is    then  unconscious  of    his    n  a   when  attention  is 

'      Hi   in ,-,    oi  may  not  l»'  able  to  read  and  writing  is  impossible  or  very  defective. 


DIAGV'-I- 


n  Is   in    speaking,  uses    the  wrong    word,  puts  words  m    a  wrong  place  in  the  aentenci    and 
even  jargon 


on  memories.  Ili>  arm  and  hand    are  nol    paralysed  for   other  movements.     \ 
'  pp  words  in  the  -■  □  i  it  writing  bi mes  incoherent. 


:     1077 


Motor  Aphasia  <t  Aphemia  (221,    771 
1390 


Iphasia.  Auditor]     772 

Aphasia.    \\  ord  I  teafnees  222 
L345). 

Visual  or  Optic  Aphasia.     Alexia      77:: 
Word  Blindness  (228,  L391  . 


Mixed  Aphasia  (224) 


Paraphasia    226  77.". 

very   ran-      Agraphia  [227    t  189  778 

Paragraphia  (226  777 


foundation,  not  onlj  of  the  mo  I  iu  ,,i  jpeeoh,  but  als erebral  localisation 

each: 

'li  full  understanding,  bul  can  oopj      irrectly  and  understands  wh  him 

•  I.  write  and  understand   •  him. 

nd  can  undo  and  writing. 

111  dictation,  nor  read  aloud  perfectly,  n  «  sj h  or   • 

li. 

lictation,  and  read  iloud,  bul  all  without  unda  I  cannot  understand  aithet  q h  w  writing 

:ny- ,'!'  idersmotoi  aphasia  to  I mbinationoi  wnson 

article  had  ,ni.ki... 


CHART  XIII  c 

Disorders  of  Gait;  Ataxic,  Paralytic  and  Flaccid,  Para- 
lytic and  Spastic  Gaits 

1  omprimng  Numbers  7:>ti  to  742  on  left  side  of  Chart 
and  780  to  800  on  right  margin 

Note) — In  addition  to  the  diseases  mentioned  in  this  chart,  pain,  whether  in  the  joints 
(rheumatism,  gout,  arthritis,  morbus  coxae,  etc.),  or  in  the  muscles  (rheumatism,  myositis, 
■  tc  or  in  the  bone-  (caries,  etc.),  or  in  the  nerves  (Bciatica,  etc.)  will  cause  a  limping  unit.  The 
gait  of  a  patienl  suffering  from  weakened  arches  in  the  feet  is  very  characteristic  in  advanced 

and  this  common  disease  Bhould  always  be  though!  of  in  anj  disturbance  of  gail  and  in 
any  painful  affection  of  the  legs  or  lower  back. 


161 


DIAGNOSTIC  ANALY  S 


DIAGNOSTIC  SYMPTOMS  AND  TESTS 

The  disorder  is  of  a  temporary  nature     Patient's  speech  is  blurred  and  foolish. 


710 

\i.i\i:i       In- 
coordination 

is    tlic    must 

prominent 

symptom. 


Staggering 
Gait.    (Reel- 


Disease  of  permanent  nature.    Patient 

Bways  from  side  to  side  and  lurches 

like  a  drunken  man.    The  ataxia  is 

almost  entirely  limited  to  walking 

(_     and  standing. 


There  is  a  strong  heredity  and 
di  ea  ie  occurs  in  family  groups  and 
in  youth.     Nystagmus. 

I  No  heredity.    Occurs  al  anj  age. 


DISORDE 
ABSTRACT 
Marked  men 

Ooours  liefoi 

Occurs  aftei 
optic  atri 

Retract  ion  o 


[nooordi- 
nated  I  rail 
Stamping 
gait.) 


Waddling 
Gait. 


Patient  does  not  walk  like  a  drunken  man,  but  throws  his  lens  about  in  an  awkward  and  excesi 

manner.      All    movements  of   legs   are  ataxic.      In    well   marked   cases   legs   arc   raised   high,    II 

outwards  and  forwards  excessively  and  brought  back  and  down  to  ground  with  hard 
heel.     The  eyes  are  employed  to  control  the  movements  and  walking  in  the  dark  is  very 

perfect  Or  impossible. 


Muscular   atrophy    and    pseudo-hyper- 
trophy. 


Muscles  normal. 

General  weakness,  especially  of  extensors 


High-step- 


r 


In  walking  patient  throws  body  from  side  i"  side  lil 

weak.      In   rising    patient    pushes    himself  up  with  fa 

tumors. 

Similar  walk.    Congenital.     Usually  bilateral  but  ma 

of  hip  and  absence  of  acetabulum. 
Bilateral.      May  be  si ataxia  in   the   walk.      Mil 


DISORDERS 
OF  GAIT. 


7)1 

Paralytic         nine  Gait       (Weakness  of  extensors  only.     Bilateral.     Blue  line  on  gums.     Wrist-drop  as  well  as  foot-dro] 

and    flaccid.      ' 

CWeaknt  Variable  distribution.    Weakness,  especially  of  extensors,    often  unilateral.     Muscular  atro] 

the  most  pro- 
minent 


>v'"1'1 Feel  drag         to   walking  all   muscles  of  leg:   -,,„ 

nvi'i  ground.       too  weak  to  raise  feet.     No  tremor 
or  spasm.     Steps   short. 


Hysterical      symp- 

Inabilitv     to    V"";   I'!'"-'',',"'  Both  '"- 

-.and   on  one      -aek  of  will  power. 

or  both  fee.      Knee-jerk  may   be   -; 
increased.      Ankle- 

clornis  nsuallv 


clonus  usually, 
Babinski  always 

absent. 


i  ine  leg 
Unilateral. 


742 

(BtiaSStM.  *«&    Legs 

hi„^,J  r'^'1  w»dfre- 

'""-  quently 

minent  '       ,  ■• 
.  remble. 

symptom. 


Tendon  reflex. 
creased.  Ankle-    , 

and      Bab 

inski  pre  i  at 


("Temporary  condition  following  .linos.    Organic  and 

Permi nt  condition,    Organic  and  peripheral  reflexes 

1     disease. 

1  Advanced  Age,  atheromatous  aj  teries      Loss  of  memo 

Legs   can   be   moved   freely   and   normally   when   lyii 

walk  or  has  forgotten  how  to  walk 
The  weak  leg  is  drawn  along  after  the  strong  oni 

Strength   in   leg   than   would   be   necessary   for   wa 
I  Sclmllor's  side  gait  I. 

The   weak    leg   is   usually   Swung   forwards  and   oiit\ 

leu  is  usually  strongly  extended  at  the  face  and 
laterally)  along  a  line  the  patient  moves  well  bo 


The  lens  are  rigid  and  offer  resistance  to  forwar. 
walking,  bodj  and  -boulders  .nils,  often  be  !»■ 
legs  forwards.     Legs  frequentl}    show    tremblin 

forward.      Thighs  are   adiiucleii   BO    that    knees   a 

!  in  walking  (scissors  gait).     Pernici 
of  severe,  anemia   maj   be  present, 


i  rigidity. 


Patient  is  slightly  bent  forward    and  all  bis  joints  slightly  Hexed. 

enq    to  Staggci   backwards        l':i>  sivc  .  rumor 


Fes  tin 


5  OF  SYMPTOMS 


OF  GAIT 
SYMPTOMS 
disorder  and  history  of  alcoholic  abuse. 

Aberty.     Krfee-jerka  usually  present.    Contracture  and  deformity  of  feet.     Babinski  present. 

jberty  but   in  youth.     Knee-jerks  usually  present   and  exaggerated.    Oculo-motor  paralysis  and 

•ml,  cerebellar  fits  and  other  cerebellar  symptoms  may  be  present. 

f  Knee-jerks  abolished.     Argyll-Robertson's   phen  imenon,   optic  atrophy.     History  of  syphilis 
usually.     A  common  disi 
Knee-jerks  are  usually  present.     May  be  no  other  symptoms  than  ataxia  and  anesthesia,  or 
may  bo  all  the  spinal  symptoms  of  locomotor  ataxia   but  none  of  the  crania  ,  especially  no 
eye  symptoms,     A  rare  disease. 

i  duck.     Marked  lordosis.     Atrophy  of  some  muscles,  apparent  hypertrophy  of  others,  but  all  are 
.anil-  and  crawls  up  his  own  legs.      A  similar  gait  is  Been  al  times  in  pregnancy  and  in  abdominal 


DIAGNOSIS 

Alcoholic  Intoxication  (658,  663,     780 
673,  764  . 

Friederich's  or  Hereditary  Ataxia    781 
(652,  urn  687,  762 

Marie'- or  Hereditary, Cerebellar    782 
Ataxia    651 

rebellumoritBtractE 
(609-10.  tils  686,  1016,  1272 

661,  766,    827    894,   979,     784 
'is;,  nmt.  1217,  1231 
24-7. 

Lesions  of  p  isterior  columns  of    786 
spinal  cord  (654a,  1347,  1350-1, 


Muscular  Dystrophi 
L152). 


786 


teral.     No  change  in  the  muscles.     Hip  joints  unusually  mobile      X-ray  shows  dislocation 

lar  weakness,  tenderi and  atrophy      Knee-jerks  absent.     Man]  sensory  symptoms. 

if  colic  and  of  exp  '-'in-  in  lead. 
without  tenderness      Electrical  reaction  of  degeneration.     No  sensory  symptoms 

Sexes  normal.     No  sensory  paralysis 
!    lost  .     Sensory  paralysis     Patients,  even  with  crutches,  are  rarely  able  to  walk  in  this 

in. I  mental  impairment.     Reflexes  normal  or  increased. 

•r  sitting     Patient  apparently  makes   no  effort   to    walk.     Legs  collapse.     Apparently  is  afraid  to 


ntal    Dislocation   of   the     786a 
Hip. 

Multiple  Neuritis    188,  662,  823,     7s7 
1008,  1117.  1307  . 

Lead  Palsy    194,  1050  ,  7ss 

Acute  Anterior  Poliomyelitis  1 195,     789 

11  Is.    I 

Weakness  671  790 

Myelitis    or     Myelomalacia    in    7"*  •  1 
lumbar    enlargement    of  cord 

is".  825 

Senile  Parapli  gi      522).  791a 

i  and  Vbasia    287   653  792 


aslvai -   beyond     it.      In    some    action-    when    taken    unawares    the    patient    shows    more 

g.     In    walking    sideways    stepping  laterally)  along  a  line  patient  moves  badly  in  each  direction 


1  Hemiplegia 
legia  1 1074 


it  the  normal  leg  as  >  pivot  and  i-  set  down  in  advance  of  tin-  latter  (mowing  gait  The 
•  whole  side  of  the  body  i-  rigid  and  swings  forward  as  a  whole  In  walking  sideways  stepping 
il.-  the  paralysed  Bide,  but  badlj  towards  the  healthy  Bide  (8chuller,«  side  gait), 

Organic  reflexes  are  disordered,  and  sensor]  symptoms  are  present,     No 


Aramenl  '    o  t b-  t   in      Organic   reflexes   maj    or    may    not    be  disordered,    sensor]    symptoms 

r-kwards    to'   pull 
lien   brought 


u-ld    tiuhl    togcthei    ■  ,.  iii 

n      f  Organic    reflexes   no     di 

Bj  mpi 


(■At 

■ 


\diilt 
mill.     Scissors  <  hut. 


Intention  tremor,  marked  ataxi  i.  at  times  staggeriE 
■n  md  prop  ni  i'  ever  increasii  ipul  lion    ■  tend- 


jplegia  or   Monop-    794 

plexy,    <  'erebral   or 

Spinal.  Tumor  01 

Myelitis  or  Myelomalacia  above    796 
lumbar  enlargement,  including 
Compression  Mvelitts  (517-20, 

J  1-7 

includ-    797 
ing       Vmyotrophii        i 

■  17 

Cerab 

lllls 

1170,1187,  i 
or        M  iltipl 
Sclerosis   (511     580 
688,  I 


CHART  XIV 

Disorders  of  Sensation 


DIAGNOSTIC  ANALYSIS  OF  SYMPTOMS 
DISORDERS  OF  GENERAL  SENSATION  AND  OF  THE  SPECIAL  SENSES 


Symptom 
Analysed 


Alterations  in  Sensation 
'810 


Mil 

Disorders  of 
Sensation. 
(See  also 
Perversion 

of  Sensa- 
tion (.'hart 


805 

Diminution  of  Sensation. 


806 

Exaggeration  of  Sensation. 


807 

Disturbances  of  Vision. 


SOS 

I  •isturlianccs  of  Beating. 

809 


Anesthesia  and  Analgesia. 

811 

Dissociation  of  Sensation. 

812 
.  Loss  of  Muscle  Sense. 

813 
Hyperesthesia. 

fS14 
Perversion. 

815 

Limitation  of  field  of  vision.  . 

816 

Double  vision. 

817 

Conjugate  Deviation  of 
Eyeballs. 

818 

Pupillary  Abnormalities. 

819 

<  >!>litimlinoscopic  Exami- 
nation. 


.  See  Chart  XIV  a. 


See  Chart  XIV  b. 


tSee  Chart  XIV  <■. 


See  Chart  XIV  .1. 


f820 
Deafness  (anakusia). 
821 
Hyperakusia  (oxyakoia)  or 


See  Chart  XIV  .-. 


Disturbances  of  Taste  and  Smell.  I      Parakusia. 


163 


CHART  XIV  a 

Disorders  of  Sensation 

<  lomprising  Numbers  806  to  812  on  left  side  of  chart 
and  822  to  841  on  righl  margin 


I  US 


DIAGNOSTIC  SYMPTOMS  AND  TESTS 


■Tendon  reflexes  diminished  or 
absent  i  lesion  of  peripheral 
sensory  neurons — 472). 


SOS 

DIMINUTION  OF 
CUTANEOUS 
SENSIBILITY 
(345  . 


Sill 

\\l  VI 'llKSIA\"usu:illv  n.m- 
bitoed  with  Borne  ANALGESIA 
and  THERMIC  ANESTHE- 
Sl  \.  especially  in  severe  cases 
of  the  disease  (348^0).  (Figs. 
■Ji;,  33). 


Organic  reflexes 

normal  (300). 
(Figs.  24-6). 


Organic        reflexes 
disordered  (300) 
(Figs.  21-7 


Organic         reflexes 
disordered:  it   may 

I ni\  slightly 

(300). 
(Figs.  19-30.) 


I 'I'll. 


Tendon  reflexes  normal  or  ex- 
aggerated   in    arms    or    legs  ■ 
or    both    (lesion    of    central 
sensory  neurons — 473). 


fAss, 
mi  il 


Organic  reflexes 
usually  normal 
very  rarely  disor- 
dered (300). 


Tendon  reflexes  absent  in  arms; 
exaggerated  in  legs.  Lesion 
both  of  peripheral  and  of 
central  Bensorj   neurons. 


<  trganic 
slightly 
(300). 


reflexes 
lisordered 


Ml 

ANALGESIA  and  THERMIC 
ANESTHESIA  with  little  or 
no  TACTILE  ANESTHES1  \ 
DISSOCIATION  OI  SEN- 
SATION    (365). 


BIO 

AKINES1  III  -I  \ 


Tendon    reflexes    usually    exag- 
gerated in  legs  I  173).    <  trgamc    - 

relieves     little    01     not     al     a] 

disordered  (300). 


Arms  affected. 


Leg    affected. 


A 

hyst 

ton 


I'M 
\ 


NUMBNESS. 


806 

EX  UJGERATIONOl  <  i  TANEOUS  SENSIBIL1  I  5 


Motor  paralysis  and  hyper 
opposite  sale  of  i he  bod) 

Loss  of  muscle  sense  is  usually  associated  with  ataxia  and  an 
pai  ietal  cortex. 

Unilateral  numbness  of  hand  and  foot,  steadily  progressive, 
Bilateral  Dumbness  i-  of  no  diagnostic  importance      It    may 


Hyperesthesia   and  hyperalgesia  ari 
myelitis. 


if  little  or  no  diagnostii 


DIAGNOSTIC  ANALYSIS  OF  SYMPTOMS 


ANESTHESIA  AND  ANALGESIA 

ABSTRACT  OF  SYMPTOMS 

esthesia  corresponds  to  the  distribution  of  a  nerve  or  to  that  of  one  of  its  branches,  though  usually  less  extensive.     In  case  of  spinal  nerves  there  is  also  a  paralysis  of  motion, 
is  pronounced,  in  the  distribution  of  the  nerve  (Figs.  33-38). 

esia,  pain  and  muscular  paralysis,  tenderness  and  atrophy  widespread  and  symmetrical  in  the  distribution  of  spinal  nerves.     Usually  a  history  of  alcoholic  abuse. 

esthesia  corresponds  to  the  distribution  of  a  nerve  root,  but  is  less  extensive.     Central  symptoms  often  present  (Figs.  33-38). 


ted  with  flaccid  paralysis,  muscular  atrophy  and  trophic  disturba 
iling.     Incontinence  of  feces.     Bedsores. 


legs.     Bladder  empty  and    j  Symptoms  bilateral.     Acute  or  sub-acute. 

[_ Symptoms  mainly  unilateral,  at  least  at  first.    Very  slow  progressive  course. 

tor  paralysis,  but  marked  ataxia  and  loss  of  muscle  sense.     Romberg's  symptom,  Argyll-Robertson's  pupil.     Tabetic  cuirass.     Retardation  of  conduction  of  pain.     Optic  atrophy 
ent.     Ulnar  hypesthesia  and  paresthesiae. 


ted  with  spastic  paralysis,  without  muscular  atrophy,  ii 

il  anesthesia  bounded  above  by  a  zone  of  hyperesthesia. 


and  legs,  or  in  legs  alone.     Bi-     fSPastic  Paralysis  in  both  arms  and  legs, 
(Spastic  paralysis  in  both  legs. 
ted  with  paralysis  of  cranial  nerves,  ataxia,  symptoms  unilateral,  at  least  in  early  stages,  dysarthria  and  dysphagia. 
tor  paralysis,  anesthesia  limited  to  anal  and  genital  region  and  vicinity.     Incontinence  of  urine  and  fece3.     Impotence.     Reflexes  in  legs 


Priapism.     Disturbances  of  respiration. 


ted  with 

.ymptoms 


ted  with 
:al  symp- 
25). 


nly  irri-    (  Motor  spasm  {retraction  of  neck  and  opisthotonus)  and  convulsions.     Acute  onset  with  fever.     Kernig's  sign.     Lumbar 
(      puncture  shows  globulin  and  increase  of  cellular  elements  in  cerebro-spinal  fluid.     Herpes  facialis. 

Motor  paralysis,  which  may  be  temporary.     Often  hemianopia.     Usually  ataxia  and  loss  of  muscle 
sense.     Cerebral  symptoms.     Post-hemiplegic  motor  disorders. 


Symptoms  unilateral.     Mainly  para-     f  Acute  onset. 
I     lytic.  J 

^Chronic  onset. 

Symptoms  usually  unilateral.     Anesthesia    usually  in  form  of  hemianesthesia,  which  may  be  transferred  in  some  cases.     Anesthesia  often  bounded  by  a  prominent       Hysterical  Anesthesia  (1074). 
anatomical  landmark.     The  anesthesia  is  usually  unknown  to  the  patient  and  is  discovered  upon  physical  examination,  but  when  discovered  is  usually  more  com- 
plete than  that  present  in  cases  of  organic  disease.     The  anesthesia  is  not  real.     The  patient  can  button  clothes,  etc.,  with    anesthetic    hands    without    looking. 
No  evidence  of  any  organic  disease. 


Usually  motor  paralysis.     Convulsions,  local  or  general.     Jacksonian  epilepsy  (587, 
inertia  and  impairment.    Choked  disc  or  optic  neuritis. 


DIAGNOSIS 
Neuritis  or  Nerve  Injury  (489,  492,  941,  1146-7,   1173,  1301-7). 

Multiple  Neuritis  (4SS,  662,  787,  1008,  1147,  1307). 

Lesion  of  Posterior  Nerve  Root  or  of  Spinal  Segment  (1302). 

Myelitis  or  Myelomalacia  in  Lumbar  Enlargement  (4S5,  791,  1309). 

Tumor  in  Lumbar  Enlargement  (486,  1309). 

Tabes.     Locomotor  Ataxia  (661,  753,  784,  894,  979,  937,  1004,  1217, 
1231). 

Myelitis  or  Myelomalacia  in  Upper  Cervical  Region  (513-4). 

Myelitis  or  Myelomalacia  in  Dorsal  Region  (517-8). 

Lesion  in  Brain  Stem  (535,  653). 

Lesion  of  conus  terminalis  of  Spinal  Cord. 

Cerebral  Meningitis  (508,  590,  60S,  1032,  1045,  120S-9,  1228-9). 

Cerebral  Hemorrhage  or  Softening  (504,  5SS,  S32,  856-7, 1043, 1060-4). 

Cerebral  Tumor  (507,  536-42,  578,  587,  833,  S49,  855,  861,  892,  90S, 
960,  1047). 


824 
S25 


830 
830a 
831 

832 

833 

834 


ted  with  flaccid  paralysis  and  muscular  atrophy  in  arms,  with  spastic  paralysis  in  legs.     Bladder   /Symptoms  bilateral  and  acute  or  sub-acute, 
ided  and  dribbling.     Constipation.     Pupils  are  unequal  often. 


^Symptoms  mainly  unilateral,  at  least  at  first.    Very  slow  progressive  course. 


nd  paresthesiae  : 
mds  and  arms 
chronic  course. 


arms  and    hands    are  _  prominent   symptoms.     Motor   weakness   and   tremor   of    arms.    Muscular   atrophy,   with  fibrillation 
late   stages.    Scoliosis    and  kyphosis    in  neck  and  upper  dorsal  region.     Spastic  symptoms  in  legs.     Organic  reflexes  normal. 


tabetic-like)  and  paresthesiae  in  legs  and  feet.     Le<*s  exhibit  a  steadily      fReflexea  increased  spasm  predominates  over  paralysis  in  early  stage.     Babinski  usually  on  both  sides,  but  in 
ising  paralysis,  which  may  he  unilateral  in  the  ,-arlv  stage..     Organic    J      unecmal  deSree-     Organic  reflexes  slightly  disordered. 

es  are  more  or  less  disordered.     Chronic  or  sub-acute  course.  ,  t>  n  i      u  r  u    i      t       ■     r  *     u  ■    i  ^         -a  i  i  n     j-      j      j 

(.Reflexes  early  abolished.      Tropic  disturbances  in  legs.     Organic  reflexes  early  and  greatly  disordered. 

lesia  on  one  side   of  the  body  and  extremities;  analgesia  and    thermic   anesthesia   and  at  times   also   tactile   anesthesia  on   the      Much  girdle  pain  and  spinal  epilepsy  are  com- 
ul  extremities.  mon  symptoms. 


Myelitis  or  Myelomalacia  in  Cervical  Enlargement  (549-50,  1310).         835 

Tumor  in  Cervical  Enlargement  (551,  1310).  836 

Syringomyelia   or   Morvan's  Disease  (cervical  type)   (552,  693,   1009,     S37 
1150a,  1170,  1187,  1357-9).     (Figs.  24-7.) 

Syringomyelia  or  Central  Gliosis  in  Dorsal  Region.     (552).  838 

Syringomyelia  in  Lumbar  Enlargement.     (552).  839 

Brown-Sequard  Paralysis  (442,  509,  981).     (Figs.  24-8.)  840 


hesia.    It  i 


multiple  neuritis,  tabes,  i 


lesions  of  posterior  columns  of  spinal  cord,  of  brain  stem,  of  posterior  third  of  posterior  limb  of  internal  capsule  and  of  the 

or  in  such  cases, 
due,  with  the  exception  of  the  zone  of  hyperesthesia,   limiting  above  the   anesthesia  in  transverse  myelitis  or  myelomalacia.      In  such   cases  it  marks  the  upper  limit  of  the 


h    slowly  progressive  mental  dulness  is  suggestive  of  cerebral  tumor.     So  much  so  that  "choked  disc"  and  other  symptoms  of  cerebral  tumor  should  be  i 
either  of  nervous,  or  of  vascular,  origin. 


CHART  XIV  b 

Disturbances  of  Vision 


Comprising  Numbers  807,  814,  815  on  left  side  of  <  Jharl 
unci  M'J  to  866  on  right  margin 


DIAGNOSTIC  SYMPTOMS    WD   fESTS 


DIAGNOSTIC  ANALY 


DISTURBANCE 
ABSTRACTS  i' 


814 

l-i.i:\  ERSION 


307 

DISTURBAV 
OF  VISION 


815 

ABSENCE  OB 
LIMITATION 
OF  FIELD  OF 
VISION 
(368  to  364). 


\  yellow  color  of  .'ill  objects  seen  irrespective  of  thru-  true  color:  xanthopsia  (yello 
A  red  color  (erythropsia)  of  all  objects  seen  irrespective  of  their  true  coloi    red  vi 

A  green  color  of  all  objects  seen  irrespective  of  their  true  color  (green  vision). 
Muscae  volitantes,  twisted  threads  and  irregular  spots  moving  about  in  Geld  of  v 
j  Flashes  of  light  and  dark  spots  surrounded  by  a  bright  zone  (glittering  jcotomata 
Achromatopsia  (364)  and  heinichromatopsia  occur  in  slight  lesions  of  the  geniculate 


An  inversion  (red  having  a  larger  field 
than  the  blue — 14)  and  an  interlacing, 
of  the  color  fields    (Dyschromatopsia). 


Blindness  (358, 


r  Bilateral. 


1318).      No   lesion    -\  TT  •■  .       , 
-mlI uu  Unilateral 


within  orbit 


Bilateral. 


Homonymous  Tetartanopia  or  Quadrant 
Hemianopia. 


("Hysterical  symptoms  (425)  arc  present. 

|  Choked  disc  and  other  symptoms  of  br 
I     creased  intra-cranial  pressure  is  relie 

No  lesion  in  eye.     Pupillary  reflexes  not 

No  lesion  in  eye.     Optic  neuritis  may  b 

No  lesion  in  eye.     No  optic  neuritis.     1 
k     shown  that  the  blindness  is  not  real. 

No  hemiopic  pupillarj  reflex.  No  hen 
or  other  paralysis.  May  or  may  not 
disc.  Very  rarely  occurs  in  lesions  of 
or  optic  fasciculus  of  opposite  side 


No  hemianesthesia.      N»^XS 


Homonymous  hemianopia  (14,  362,  1321). 
May  very  rarely  be  bilateral,  due  to 

double  lesion. 


Bitemporal  hemianopia  (362,  L319). 

Nasal  hemianopia    362,  1320). 

Horizontal  hemianopia. 
Bomonymous  seotomata, 


Hemianesthesia. 


May   or   may    not    be   a   hemiplegia. 

pupillary    reflex.      Paralysis    of    mote 
:il>duccn>    ner\  e  or   both. 


Slow  onset,  progressive  course,  terminal 
in  complete  blindness.  Choked  disc 
pupillary  reflex. 


Occurs  in  lesions  of  the  retina,  or  of  opt, 

These  may  occur  as  the  result  of  small 
neighborhood  of  the  calcarine  fissure. 

("Increased  tension  of  eyeball.      Excavati 

t'upph 


Concentric  limitation  of  field  of  vision,    J  N?  ««™wed  *****  of  eye-      On  ophl 
even  to  complete  blindness. 


Hysterical  symptoms  (425)  are  present 


Symptoms  of  tabes  are  present,  esp 
no  ataxia.     History  of  Syphilis.     '  [lob 


OF  SYMPTOMS 


DF  VISION 
rMPTOMS 
poo 


d  especially  when  eyes  arc  turned  towards  a  bright  light, 
iddenly  appearing  and  disappearing  in  the  field  of  vision, 
lies,  of  the  optic  fasciculus  and  especially  of  the  calearine  cortex. 


ire  present       I'h ilor  lield  becomes  normal  after  the  in- 

<  Pushing.) 

I  remic  amaurosis  may  be  in  this  class  (edema). 

Pupillary  relic 

Uary  reflexes  normal.     Hysterical  symptoms.     By  tests  it  may  be 

luadrant  of  each  field  of  vision. 
i 
I       Lowei   In  u'li  field  of  i 


DIAGNOSIS 

Jaundice,    or    Santonin,    Arayl    Nitrite,     Cannabis     842 
Indica  or  Picric  Acid  Poisoning. 

Neurasthenia,  Hysteria,  great  emotional  excitement     343 
and  after  cataract  operations;  also  after  the  eye 
has  been  exposed  for  a  long  time  to  an  electric  or 
other  bright  light  (snow-blindness). 

Diseases  of  optic  nerve  and  retina  and  after  cataract    844 
operations. 

Neurasthenia,  circulatory  disturbances  in'brain  and     845 
digestive  disturbances. 

Migraine,   and  Aura  of  Epilepsy,   and   circulatorv     846 
disturbances  in  brain. 


Achromatopsia 
Hysteria  (1074). 
Cerebral  Tumor  (833). 

Lesion  or  edema  of  both  occipital  lobes. 
Lesion  of  optic  nerve  or  chiasm. 
Hysterical  Amblyopia 


847 
848 
849 

B60 

851 
851a 


Lesion  of  lower  lip  fissure.     852 

Lesion  of  upper  Up  of  contralateral  calearine  fissure. 


I  Sudden  onset   and  of  -hort  duration.     Often  more 
|      marked  in,  or  limited  to,  one  eye.    No  other  syuip- 
'•xcept  nervousness.    Circulatory  disturb 

Choked  disc.     Slow   onset.     Progressive  course  of  the 
'  disease. 

No  choked  disc.    Rapid  onset.    Permanent)  not  pro- 
hows  a  regressive  - 

No  hemiopio  pupillary  reflex.     No  choked  disc.     Re- 
gressive course. 


miopia 

mil    or    •' 

N 


■ 


.  No  ohoked  disc     Rapid  onset.    Symptoms  of  menin- 

l    gitis  may  be  present. 


1 


involving  their  upper  or  lower  p  ■ 

'IIS     ill    tfa 


Aura  of  migraine. 


854 


Tumor   involving   median    surf:. 
occipital  lobe  or  fasciculus  of  Grate 

Hemorrhage  or  softening  in  or  near  contralateral  cal 
carin  ciculus  of  <  Irat 

orrhage  or  softening  in  the  posterior  pari  ol 
terior  limb  of  contralateral  internal  capsule. 

Tumor  involving  contralateral  optic  tract  or  geni 
ulate  bodies 

Neuritiaor  lesion  of  contralateral  optia  tract   [898 

Tumor  oompi  tral  part  of 

(8!>l\  I  pituitary.) 

Tumor  compressing  homolateral  outer  part  of  optic    sci 
392,  i  I  !0 


I  >|ila 

Horn  i 


tnd  final  atrophy  ptic  nerve.     Pupi  aid  mutual ,      i  MS), 

'"-'"I' > aniin  ition  ti ptic  papilla   ihowa  itrophy.  Optio  atrophy. 


864 


■gvii-i;  h.'m  ' -  in'  i  phenomenon  and  ibseno  eof  reflex 
and  lymphooytosia  In  cerebro-apinaJ  fluid. 


Little  or 


CHART  XIV  c 

Disturbances  of  Vision 


DIAGNOSTIC  ANALYSIS  OF  SYMPTOMS 


Character  of  the 
Diplopia 


Secondary 
Deviation 
of  Sound 
Eye  (29) 

Inward. 


807 

l> 

I 

S 
I 
I 
K 

B 

\ 

I 

l. 

0 

I 

v 
1 

s 
I 

0 

N 


S16 

Double 
■.  iaion. 
Diplo- 
pia 

(Fig.  18) 


The 
images 
separate 
and  come 
together 
again 
when 
the  eye- 
lolls  are 

from  one 
side  to 
the 

other,  or 
upward 
or 

down- 
ward 
and  back 
again. 


Displace- 
ment of 

Visual 
Axis  (28) 

Inward.  Strabis- 
mus convergens. 


Outward.  Outward.  Stra- 
bismus diver- 
gens. 


Limita- 
tion 


Outward. 


Inward. 


Graphic  Represen- 
tation op  the 
Diplopia. 
Broken  Line  is  the 
False  Image 


Upward. 


Down- 
ward 


Down- 
ward 
and 

inward. 


Upward 

and 
inward. 


The  A 

together 

eyeball* 

are  i  ur I. 


1  low  nward. 
Strabismus 
deorsum  ver- 
gens, slightly 
divergens. 


Upward.  Stra- 
bismus sursum 
vergens,  slightly 
divergens. 


None  or  slightly 
upward  and  in- 
ward. Strabis- 
mus sursum  ver- 
gens, slight  ly 
convergens. 

None  or  slight  ly 
downward  and 
inward.  Stra- 
bismus deorsum 
vergens,  slightly 
convergens. 

May  be  variable. 


Position 
of  False 

Image 
(See  28) 

On  the  same 
side  as  the 
affected  eye. 

On  the  oppo- 
site side  to 
the  affected 
eye. 


Upward  Above  and  on 
and  opposite   side 

somewhat    to  the  affect- 
inward,        ed  eye,  image 
tilted  top  in- 
ward. 

Down-  Below  and  on 
ward  and  opposite  side 
somewhat  to  the  affect- 
inward,  ed  eye,  image 
tilted  top  out- 
ward. 

Rotation  Below  and  on 
downward  same  side  as 
and  the     affected 

somewhal   eye,       image 
outward,      tilted  top  in- 
ward. 

Rotation  Above  and  on 

upward  same  side  as 

and  the      affected 

hat  eye.        image 

outward,  tilted  topout- 

ward. 

FUt.  ii 

The  limitation  of  motion  and  the  ] 

of  the  I     !  !  he  reverse  of  those 

in  paralyeis.   There  may  be  present 
irritation,  especially  in  t  be  nose  or  teeth, 
which  wonl.l  cause  a  reflex  spasm.    The 

spasm   is   usually   more  transient    tl 

are  MM  internal    rectus  and   the     inferior 
oblique. 


a 

u 

u 

a 

I 

k 

1 

i 

I 

>i 

1 

I 

e1 

K 

i 

<> 

i 

Diagnosis 


Ex-    870 

ternal 

Rectus. 

In-     871 

lernal 
Ueci  us. 


Su-     872 
perior 

P      Rectus. 

A 

H 

A 

L 

Y 

S 

I 

S 

0 

Y 


In-      873 
ferior 

Rectuv 


Su-     874 
perior 
Ob- 
lique. 


fa-      ST.-. 
ferior 
Ob- 
lique. 


The  whole  eyeball  can  he  seel,  to  he  displaced. 

r/No  changes  visible  in  eye.      Hysterical  sympti  represent. 

"Two  openli  en  in  pupil. 


MONO- 

Cl  LAB 


ill  eve 


Spasm  of  the    B7fl 

ooular  n. 


Displaoemenl    ^77 
ol  eyeball. 

ioal        ->7^ 

diplopia. 

Double  pupd-  B78 


By  oblique  illumination  the  lens  can  be    Cataract. 

teen  to  be  opaque  in  p 

Examination  show-  dislocation  of  lens.         Dislocation       sxi 


Examination  shows  astigmatism  and  an 

irregular  contour  of  the  cornea. 


Dislocation 
of  lens, 
[rregularit 


B17 

i  onjugate 
deviation 


•  l  » ith  oiler  m    m.jr    the    anterioi  883 

Deviat   in  I    u    i  llj  do    pn   snt     portion  of  the  pons  (otphs 
when  the  eyeballi  are  at  rest.    A  vertical  deviation  I)  to  the  abduoens    du 

itcil  with  a  lesion  "t  the  corpora    clous,    involving    posterior 


quadrigemin  i 


I  w  it  h  other 
symptoms    ol 

ol    ill.-    b 


i    tl.e 


longitudinal  bundle. 

aj   884 
part    of   brain,  espsoially,  In 

■  r  part  of  frontal  loin' 

e    lesion   In 

cortex. 


CHART  XIV  d 

Abnormalities  of  Pupil  and  Optic  Papilla 

Comprising  Numbers  818,  819,  890,  891,  897  and  898  on  left  ride  of  ( 'hart 
and  890  to  914  on  right  margin 


171 


DIAGNOSTIC  ANA  J 


Ms 

ABNORMALITY 
OF  PUPIL 


819 

U3NORM  \l.l  I  5 

"I    PAPILLA 

Result  of 

i  tphthalmoscopii 

I  lamination. 


DIAGNOSTIC  SYMPTOMS   \NI>  TESTS 

Disordered  pupillary  reflex  to  light  and  accommodation  (330-1). 
Mydriasis,  myosis  or  unequal  pupils  (339-41), 


Sill  I 

The  hemiopic 
pupillary  reflex 
[26). 


891 

The  Argyll- 
Robertson 
phenomenon  (447). 


Bitemporal  bemianopia  (362,  1319). 
Homonyi is  hemianopia  (362,  L321). 


History    of   syphilis.      Lymphocj  toai 
in    cerebrospinal  fluid. 
Positive  Wassermann. 


897 

i  Iptic  neuritis. 

Choked  disc. 


Bilateral 


trophj . 


i  oilateral 


Bilateral. 


I  Inilatera 


PUPILLARY  ABNORMALITIES  A 
ABSTP.  k.CT  OF  S 

These  phenomena   oocui  in  to< 
Their  significance  ha    b< 

( 'linked  disc.     Symptoms  prof 


i  M'tcu  hemiplegia  oi  pararj  - 
history  oi  syphilis      \  erj  rai 

Vtaxia.     Absence  of  knee-jerk. 

-j  Menial  impairment.     Blurred  6 

I  Rarely  occurs.    No  ataxia     Kn 

Albumen  and  easts  in  urine. 

Sugar  in  urine  and  in  bl I 


Retinit  i 


\ arked  symp- 
toms   nf    cerebral 

disease. 


No  retinitis 


Marked  cerebral 
symptoms. 


Lead  in  urine. 


Examination  of  the  blood 
■hows  a  condition  of  severe 
anemia. 

I   line  and  blood  norm  d 


I  Well  marked  history  of  traiiinatis 

in.  rea  ed  size  of  head,  and  fonti 
Retraction  of  head.    Cerebro-ap 


General  eonvidsieu  of  Jai 
lepsy   is   common.     Maj    be 
paralysis,        Reflexes    usual! 
creased. 


Local  inflammation  can  usually  be  made  out  by  examining  thi  i       rai 

Secondary.  tt  may  be  the  terminal  stage  of  a  neuritis  and 

Traces  of  the  active  inflammation  (old  hemorr 

'  Old  age       I  sually  at  heromatous  arteries  and  liiu 

Primary.    No  signs    | LoBS  **  knoe-Jerk'     Myosis.     Lightning  pains. 
"i  a  former  inflam-       Unequal  pupils,     [mpairment  of  speech.    Tremo 

matioti.  ,  ..    ,  r  , 

I   liildislmess. 

1  lharacteristic  tremor  or  other  symptom  ol  thU 
Local  inflammation  or  lesion  can  usually  be  made  out  on  careful  exam 


SIS  OF  SYMPTOMS 


I  OPTIC  NEURITIS  AND  ATROPHY 

PTOM8 

Iny  conditions  to  be  of  much  diagnostic  importance 
based  in  <  Jhart   Vl>. 

Ire,  terminating  in  blindness.    Often  associated  with  acromegaly. 

■nuii.-il  nerves,     Optic  neuritis  or  symptoms  of    meningitis.     At    times  a 
d  quadrant  hemianopia  in  partial  lesions  of  the  geniculate  bo  lies. 

Ightning  pains.    ( lirdle  sensation  and  tabetic  cuirass. 

•Ii.     Apraxia.     Restlessness.    Childishness.     Uncontrollable. 

rks  present.    Maj  be  no  mental  impairment.    Normal  speech.    No  apraxia. 

Headaches,  especially  in  i ning.    Usually  edema  of  some  part  of 

body.     Dyspi a  on  exertion  and  loss  of  strength. 

Progressive  emaciation   and    lose   of  strength.    Greal    Hurst    and 
polyuria.     Large  appetite.     Dry  akin. 

Blue  line  on  gums.     Kistorj   of  lead  colic.     Wrist-drop.     History 
of  exposure  to  lead  poison. 

Dyspj ■<  on  exertion  and  progressive  weakni         Palloi   of  skin 

:iik1  mucous  membi 


DIAGNOSIS 

Tumor  compressing  the  optic  chiasm    851,  B60-1      892 
1319-20  - 

Lesion   of   contralateral   optic  tracl    or   geniculate    898 
bodies    868-9,  1321  . 

Tabes  (661,  827        Figs   _M-7.  v.u 

110 1  gag 

Syphilis  (1206).  896 

Bright's  Disease.  899 

Diabetes  Mellitus  1 1 175).        ,  ;kx) 

Lead  Poisoning  1  194,  576  584,  788,  988,  1060  .             901 

Anemia  '>r  Leukemia.  902 


of  syphilis.    Argyll-Robertson's  pupillary  reflex.     Lympho 
oytoau  in  cerebrc-epinal  fluid.    Positive  wassermann. 


«  hich  the  nerve  1 1  -  *  ~  been  injured    I  'sim 
■j  and  sutures  r » j ..-11  in  the  young, 
tymphi  irer. 


Dmplicated  with  facial  paralysis. 


a. 


11   nun    noi  l„-  fever.     \t   times  a  latent   period      Primary 

?uppu«tion  .nil  or  elsewhere.    <  (ptic  1 litis  present 

in  about  53'  0  of  ca 

No  fever      I  sualrj   steady  progre    ion      I  Iptii      1  iiriti    present  in 
about  mi',   ol  all  cases;  almost  invarial  in  tumors  in 

the  posterior  fossa.    Tumors  in  pituitan  gland,  corpus  oallosum 
and  in  the  central  convolutions,  especiallj  extra-cerebral  ti 
often  show  no  optic  neuritis. 


Syphilis  (1206).  903 

Injury.  .IIM 

Hydrocephalus    960  90S 

Meningitis  (590,  608)  906 

Cerebral  Uwcess  or  Sinus  Thrombosis  ■>n: 

<  larebral  Tumor  (507,  578  908 


''  follow  anj  "I  the  causes  ol  neuri  ,  1  above, 

s  and  exudates,  etc    can  luniallj  bi 

(<■ri.il  tonsion. 

der  diatui 

Mental  impairment      1:.   tl<     m         duuaaonab 

bi  m  tdi  out  roful  examination 

1,111 


1 •  " al    '  ige  ..1  1  Iptii   Neurit!     86  ■ 

Senile  1  Iptio  Itrophy. 

1 
1  mi 

668 

.'I       III.  I     Mil, II 


910 

•hi 
912 

•11  I 
91  1 


CHART  XIV  e 

Abnormalities  of  Hearing,  Taste,  and  Smell 


DIAGNOSTIC  ANALYSIS  OF  SYMPTOMS 


Diagnostic  Symptoms  and  Tests 


808 
D 
I 
S 
0 
R 
D 
E 
R 
S 

0 

F 

H 
E 
A 
R 

I 
N 

<; 


f820 
D 
E 
A 
F 
N 
E 
S 
S 


A 
N 
A 
K 
U 
S 
I 
A 
(355) 


-Usually 

unilat- 

eral. 

•w 

May  be 

0 

bilat- 

R 

eral.   A  " 

D 

perma- 

S 

nent 

.symp- 

A 

tom. 

N. 

D 

Bone 

con-  No 

due-  facia 

tion  paral- 

im-  ysis. 
paired. 


Abstract  of  Symptoms 

Severe  paroxysmal  vertigo  and 
tinnitus  aurium. 


No  vertigo.  May  be  heredity. 
Locomotor  ataxia  or  dissemi- 
nated sclerosis  may  be  present. 


Bone 
con- 
duc- 
tion 
not 
im- 
paired 


Maybe    fMay    be    history    of    syphilis, 
asso-        symptoms  of  meningitis,  symp- 


ciated 
with 
facial 
paral- 
ysis. 


I  to n is  of  tumor  at  base,  optic 
<  neuritis,  etc. 

I  Disease  of,  or  injury  to,  middle 
[or  outer  ear;  cerumen. 


Usually 
bilateral. 
Very  rarely 
unilateral, 
and  then 
only  a 
transitory 
symptom. 


C  Associated  with  symptoms  of  lesion  of  the 
pons  or  crura  cerebri. 


Associated  with  symptoms  of  lesion  of  the 
cerebral  cortex.  Complete  deafness  does 
not  always  occur  in  a  bilateral  lesion  of 
the  temporal  cortex. 


No  symptom 
WORDS  ONLY.  Sensory  aphasia  (222)  is  present. 


Hysterical  symptoms  (425). 
of  organic  disease. 


821 

HYPERA- 
KUSIA, 
OXYAKOLA 
OB  PAB  \- 
Ki  BIA 


ByBterical  symptoms  are  present. 


Diagnosis 

Meniere's  or  918 

Labyrinth  disease 
(650,  685,  1019). 

Atrophy  of  aud-    919 
itory  nerve. 

Tumor  or  inflam-  920 
mation  involving 
auditory  nerve 
trunk. 


Lesion  of  ear. 


Bilateral  lesion 
of  the  lemniscus. 
(Fig.  20.) 

Lesion  of  the 
temporal  cortex 
on  both  sides. 
(Fig.  15.) 

ByBterical  deaf- 

1074). 


921 


922 


923 


92 1 


Lesion  of  left        926 
superior  temporal 
eon  volution. 

(Fig.  15.) 


Hysteria  (1074).    926 
927 


Inflammatory  lesions  of  ear  or  its  neighborhood  are  Hyperemia  of 

present.  inner  ear. 

Facial  paralysis  is  present.    Low  notes  are  especially  Facial  paralysi 

painful.    Tinnitus  aurium  is  present.  (1317) 


B09 

DISORDERS     Very  little,  if  any.  diagnostic  significance  can  be  attached 

OF  SMELL  to  disturbances  of  smell  and  taste 

WI)  TASTE. 


173 


CHART  XV 

Perversion  of  Sensation:  Pain  and  Vertigo 


Symptoms  Analysed 


f931 
PAIN 

(330). 


930 
PERVERSION 

SENSATION 

IX  XKKVOUS 
DISK  ASKS 
(306). 


DIAGNOSTIC  ANALYSIS  OF  SYMPTOMS 

DISORDERS  OF  SENSATION— PERVERSION 

Location  of  Pain 

933 

PAIN  IN  NERVE 

Pain  limited  to  the  trunk  and  branches  of  one 
nerve  in  any  part  of  the  body,  except  that  at 
the  height  of  the  attack,  there  may  be  a  mild 
radiation  of  the  pain  into  corresponding  nerve 
of  opposite  side  or  into  adjacent  nerves. 

934 

PAIN  IN  HEAD.  HEADACHES  IN  NERVOUS 
DISEASE 

After  a  careful  examination  with  suitable  instru- 
ments has  proved  the  absence  of  glaucoma, 
iritis,  muscular  insufficiencies  and  other  diseases 
of  the  eye,  of  the  nose  and  its  sinuses,  of  the 
teeth,  of  the  ear,  of  the  scalp  (rheumatism),  or 
of  the  cranial  bones  (periostitis,  eariee). 


935 

PAIN  IX  TRUNK  IX  NERVOUS  DISEASE 
After  a  careful  examination  has  proved  the  ab- 
sence of  Pott's  disease,  rheumatism  of  spine  or 
trunk  muscles,  arthritis,  disease  of  breast,  peri- 
carditis, pleurisy,  aneurism,  pleurodynia,  perio- 
stitis cancer  and  other  tlimOTS,  colic  (intestinal, 

uterine,  biliary,  renal)  dyspepsia,  pancreatitis, 
appendicitis,  peritonitis,  gastric  ulcer,  gastritis, 
enteritis,  hernia.  Boating  kidney,  tubal   p 
nancy,  pelvic  inflammation,  intestinal  obstruc- 
tion, etc. 

986 

PAIN  i\  EXTREMITI]  -  LN  M  RVOUS 
DISEAS1 

After   a    careful   examination    has    proved    the   ab- 
sence nt'  any   disease  of  the   bones,   mu 

joint-.    Iiliinil    vessels   Or  -km   of   the   arms   and 
I  Ia1    font    mUSl    lie  excluded. 


See  Chart  XV  a. 


See  Chart  XV  b. 


932 
VKRTKio 


See  Chart   \\   i  . 


See  Chart  XV  ,1. 


17.5 


CHART  XV  a 

Pain  in  Nerve,  Pain  in  the  Head,  Headache 

<  lomprising  Numbers  933  and  934  on  the  left  side  of  ( 'hart 
and  937  to  966  <>n  the  rijiht  margin 


::; 


DIAGNOSTIC  SYMPTOMS  AND  TESTS 


933  The  differential  diagnosis  be- 
P  tween  neuritis  and  neuralgia 
A  cannot  always  be  made  clin- 
I  ically.     The  diagnosis  is  aided 

N         by  the  experience  that  certain 

nerves,  such  as  the  sciatic,  are 
I  more  prone  to  neuritis;  while 

N         others,  such  as  the  trigeminal, 

are  more  prone  to  neuralgia. 
N         (Figs.  33,  38). 


'A  history  of  neurotic 
heredity  or  other  evi- 
dence of  a  neuro- 
pathic predisposition, 
congenital  or  ac- 
quired, is"7  common. 
Pain  is  unilateral  and 
is  increased  by  move- 
ment and  by  expo- 
sure to  cold  or  wind, 
a  n  d  is  sometimes 
associated  with  mus- 
cle spasm.  Vaso- 
motor and  trophic 
disturbances  are  often 
present. 


rParoxysmal  pain  with 

free  intervals. 


I  Continuous   pain  with 
exacerbations. 


fPain  limited  to  the 
whole  or  a  portion  of 
the  trunk  and  distribu- 
tion of  the  trigeminal 
o  r  occipital  nerves. 
Diseases  of  the  eye, 
the  nose  and  its  sinu- 
ses, the  teeth,  the  ear, 
the  scalp  and  the  bones 
must  first  be  excluded. 
(For  the  diagnosis  be- 
tween neuritis  and  neu- 
ralgia see  933.) 

Pain  strictly  limited  to 
one-half  the  head. 


Never  any  motor  paralysis    or    persis- 
tent anesthesia  or  loss  of  reflexes. 


May  be  motor  paralysis  or  anesthesia 
or  loss  of  reflexes  or  all  combined. 


May  be  some  v. 
of  the  hair. 
or  neurastheni 


May  be  both  vi 
disturbances  a 
the  electrical 
tion.     General 


'The  pain  is  felt  above  the  eye  in  the  forehead,  in  the  ten 
If  tension  of  eyeball  be  increased,  examine  eye  for  glauc 

The  pain  is  felt  below  the  eye  in  the  cheek  and  side  of  nc 

The  pain  is  felt  in  the  lower  jaw  and  its  teeth  and  gums  : 

The  pain  is  felt  in  two  or  three  of  the  situations  describe! 

The  pain  is  momentary  in  duration  and  is  associated  wit] 

The  pain  is  felt  in  the  occipital  region  running  up  along  oi 
and  early  symptom  in  neurasthenia  and  nervous  breaki 

Periodical  attacks  (often  occuring  at  menstrual  epoch)  of 
crania  angio-paralytica)  or  pallor  and  dilated  pupils  (h 
there  are  vomiting  and  nausea.     The  disease  usually  e< 


Pain  as  if  nail  was  being  driven 
through  the  skull. 


Pain  of  great  intensity  in  a  small  spot  anywhen 


Pain,     nocturnal, 
small      area 
spreading. 

Pain  localized  in 
..small  area. 


Evidence  of 
poisoning. 


Evidence    of  circula- 
tory disorder. 


Evidence   of   nervous 
exhaustion 


History  or  other  evi- 
dence of  syphilis. 

Disease  exists  in  organs 
within  the  head  or 
body. 

Exogenetic. 

»  Auto-genetic. 

Cerebral  hyperemia. 
i  Cerebral  anemia 


Evidence    of 

brain  disease. 


Chronic  headache. 
Pain  constant  with 
exacerbations. 


PYREXIA.  Evidence  of  infect  ion.       Headache. 

HYPER- 
PYREXIA..^    Evidence  of  exposure  to  high  temperature. 


Pain  may  be  felt  at  any  time  but  is  worse  in  evening  or  i 
Cranium  is  often  tender  at  points.     Pain  may  be  due  t  \ 

Frontal  headache  may  be  due  to  gastric  dyspepsia  and  co 
to  pelvic  disease.     These  referred  pains  are  associated  v 

f  Occurs  after  the  ingestion  of  narcotics.     Does  not  come  on 

[  Occurs  as  the  result  of  breathing  for  hours  foul  air  in  unve 

Occurs  as  the  result  of  constipation,  especially  where  the  t 

Occurs  in  Bright's  disease,  usually  is  worse  when  patient  I 

Headache  with  fulness  and   throbbing   in    head,    aggrava 
aches  may  be  followed  by  a  cerebral  hemorrhage.     Hoa< 

Headache,  most  commonly  at  vertex,  with  fainting.     Dai 
In  this  as  in  other  forms  of  headache  several  etiologica 

Headache  associated  with  phobias  and  tremors  and  insomnia  and  other  symptoms  i 
pressure  within  the  skull,  especially  pressure  in  occipital  and  cervical  region.     Hi 

Progressive  symptoms,  motor  or  sensory  or  both,  first  of  i 
cussion  over  the  seat  of  the  lesion.     Lumbar  puncture  si 

Intractable,  incurable,  more  or  less  constant  headaches.     I 
stretching  of  the  dura  mater  by  tumor,  hydrocephalus,  < 

Diffuse  pain  and  tenderness  of  scalp.     Pain  on  movement 

f  Temporary.  Occurs  during  the  first  few  days  or  first 

\  [  Occurs  throughout  the  disease  and  is  a, 

[Permanent.  \ 

[  Suppuration  elsewhere  in  head  or  bod} 

History  of  exposure  to  high  temperature.     Headache  oft 


Optic  neuritis  or 
choked  disc. 

May  follow  trauma- 
tism. 

Evidences  of    rheuma- 
tism elsewhere. 


DIAGNOSTIC    ANALYSIS    OF    SYMPTOMS 


ABSTRACT  OF  SYMPTOMS 
trophic  disturbances,  except  rarely  a  slow  blanching      Certain  points  on  the 


-motor  but  -- 

ver  any  electrical  reaction  of  degeneration.     Patient  usually  anemic 


lerve  are  usually  tender  (points  of  Valleix).  Frequently  the  parts  supplied  by  the  nerve  are  hyperesthetic  and 
local  spasms  occur.  The  neuralgia  may  be  only  one  symptom  of  a  more  general  disease  (symptomatic  neuralgia)  or  independent 
of  any  other  disease  (idiopathic  neuralgia). 


-motor  and  trophic 
there  may  also  be 
iction  of  degenera- 
jalth  usually  good. 


j  and  i 


Nerve  neither 

swollen  nor 
tender. 


f  A  tumor  may  be  felt  or  rarely  seen  with  X-ray  on  nerve. 
I 


with  X-ray  near,  and  compressing,  the  nerve. 


A  tumor  or  a  displaced  bone  or  other  substance  may  be  felt  i 
Rash  of  herpes  limited  to  distribution  of  nerve. 
Nerve  wherever  it  can  be  felt  is  swollen  and  tender.     There  may  be  an  inflammatory  focus  near  to  and  involving  the  nerve, 
back  as  the  vertex.     It  is  most  severe  along  the  nerve  trunk  but  extends  also  beyond  it  and  on  each  side.     The  tender  point  is  at  the  supra-orbital  notch.     The  eyeball  may  be  painful  and  tender. 


and  radiates  into  the  teeth  of  the  upper  jaw.     The  tender  point  is  at  the  infra-orbital  foramen. 

I  in  the  side  of  tongue,  in  the  ear  and  in  the  temporal  region      The  tender  points  are  at  the  mental  foramen  and  in  the  temple. 

bove. 

clonic  or  a  series  of  clonic  spasms  of  a  facial  muscle. 

side  of  the  scalp  to  the  vertex.  The  neck  is  stiff.  The  tender  points  are  behind  the  mastoid  process,  behind  the  middle  of  the  sterno-cleido-mastoid  muscle  and  on  the  parietal  eminence.  This  is  a  common 
n.     In  many  cases  the  pain  is  dull  and  is  a  sense  of  strong  pressure  rather  than  pain.  v 

-ere  pain,  sometimes  on  one  side,  sometimes  on  the  other  side  of  the  cranium.  Skin  is  very  hyperalgesic  and  vaso-motor  disturbances,  either  in  the  form  of  flushing,  sweating  and  contracted  pupils  (hemi- 
crania  angio-spastica)  are  often  present.  Often  ushered  in  by  visual  hallucinations  in  the  form  of  flashes  of  light,  etc.,  or  by  paralytic  phenomena,  such  as  hemianopia.  Towards  the  end  of  the  attack 
nences  in  early  life,  ceases  in  old  age  and  often  shows  a  direct  inheritance.     "Symptomatic"  migraine  is  not  infrequent  in  tabes,  paresis,  brain  tumor  and  epilepsy. 

n  scalp  with  the  feeling  as  if  a  nail  was  being  driven  through  the  skull  at  this  point.     This  region  is  tender.    Hysterical  symptoms  (425)  are  present. 


Neuroma,  (491). 

Compression  Neuritis. 
Herpetic  Neuritis. 
Neuritis,  (489,  492,  822). 
Supra-orbital  Neuralgia  or  Neuritis. 


Infra-orbital  Neuralgia  or  Neuritis 
Infra-maxillary  Neuralgia  or  Neuritis.     ] 
Trigeminal  Neuralgia  or  Neuritis.  J 

Tic  Douloureux  (602). 
Occipital  Neuralgia  or  Neuritis. 

Migraine  or  Hemicrania.     Idiopathic  and 
symptomatic,  (846,  854,  1028). 

Clavus.     Hysteria,  (1074). 


942 
J,  Trigeminal  944 
Neuralgia 
or  Pros-     945 


it,  or  occurs  only  at  night,  i 
icriostitis.     Lumbar  punctu: 


•  in  the  early  morning  hou 
i  may  show  lymphocytosis 


It  follows 
■  positive  Was; 


distribution  but  is  felt  over  a  small  area  and  extends  ( 
Optic  neuritis  may  be  present. 


■  a  wider  and  wider  circle.   Argyll-Robertson's  phenomenon  is  frequent.       Syphilitic  Neuralgia  (meningitis 


ipation,  as  well  as  to  disease  of  the  eye  or  caries  of  teeth.     Occipital  headache  and  temporal  headache  may  be  due  to  disease  of  the  eye,  teeth,  pharynx 
i  hyperalgesia  of  skin  of  same  region,  which  may  be  as  constant  and  important  a  symptom  as  is  the  pain.     The  pain  of  eye  strain  grows  worse  towards 

miediately,  often  not  till  the  next  day. 

lated  rooms,  especially  if  patient  is  accustomed  to  pure  air.    Transitory. 

els  usually  act  freely.     This  headache  is  usually  most  marked  in  the  frontal  region. 

t  wakes  up  in  the  morning.     Urine  is  usually  scanty  and  contains  albumen  and  casts.     Edema  and  gastric  disturbances  ; 


•  ear.     Vertex  headache  may  be  due  to  anemia  i 
ening,  or  follows  reading. 


by  cough.      The  congestion  may  be  active  (after  taking  amyl  nitrite)  or  passive  (heart  disease).     Vertigo  and  vomiting  may  be  present.     High  arterial  t 
•lies  occurring  at  the  time  of  puberty  or  of  menstruation  may  well  be  congestive. 


retinit's  is  often  present. 

Tinnitus  aurium.     A  series  of  such  head- 


ess  before  eyes.     Cold  hands  and  feet.     Cardiac  t 
actors  may  be  present. 


■  arterial  disease  present.     A  series  of  such  headaches  may  be  followed  by  a  cerebral  thrombosis.     The  headache  may  be  relieved  by  the  recumbent  posture. 


neurasthenia.     Pain  grows  less  towards  evening  and  is  usually  felt  in  the  occiput  or  vertex.     Feeling  as  if  a  tight  band  or  cap  were  upon  the  head  (casque  neurasthenique).     Often  a  sense   of   fulness    and 
aches  resulting  from  overstrain  (mental  or  physical,  especially  eye  strain)  may  well  be  of  this  nature. 


Eation,  later  of  paralysi; 
•s  greatly  increased  pre 


n  case  of  abscess  there  may  be  a  latent  period  and,  in  the  active  stage,  fever.      Headache   is  constant  with  intense  exacerbations.      In  rare  cases  the  skull  may  be  tender  c 
i  of  cerebro-spinal  fluid.     Such  headaches  can  be  relieved  by  the  operation  of  "decompression." 


cause  can  be  assigned.     May  be  some  mental  deterioration  or  other  cerebral  symptoms.    No  optic  neuritis.    Lumbar  puncture  will  usually  show  lymphocyto 
.    Fever  may  be  present  in  rare  sub-acute  cases. 


Apoplectic  attacks  may  < 


fronto-occipital  muscle.     Relieved  often  by  application  of  warmth.     At  times  small  tender  nodules  can  be  felt,  and  hence  the  condition  has  been  called  "indurative  headache." 
eek  of  almost  any  fever  (typhoid).     Such  headaches  may  be  due  to  the  action  of  the  toxic  substance  directly  upon  the  brain  or  indirectly  by  causing  vaso-paralytic  congestion, 
ciated  with  muscle  spasm  and  paralysis  and  local  edema  of  the  scalp  (sinus  thrombosis).     Coma.     Lumbar  puncture  will  show  lymphocytosis  and  globulin  in  cerebro-spinal  fluid. 
Latent  stage.    Convulsions  and  coma, 
followed  by  coma  and  convulsions. 


Referred  Pains  or  Symptomatic  Neuralgia, 
(374). 

Alcoholic  or  Morphine  Headache. 

Foul  Air  Headache. 

Constipation  Headache. 

Uremic  Headache. 

Congestive  and  High  Tension  Headache. 

Anemic  Headache. 

Neurasthenic  Headache,  (1072). 

Cerebral  Tumor,  or  Abscess,  or  Hydrocephalus, 
(507,  508,  965). 

Pachymeningitis  and  Chronic  Meningitis, 
(5S8,  590). 

Rheumatism  of  Scalp. 

Infection  or  Toxic  Headache. 

Acute  Meningitis  and  Sinus  Thrombosis,  (590,  1044). 

Cerebral  Abscess  (960). 

Sunstroke,  (589,  106S). 


957 
958 
959 


I 


CHART  XV  b 

Pain  in  Trunk 

Comprising  Numbers  935  on  left  side  of  <  lharl 
and  970  to  990  on  right  margin 


L79 


DIAGNOSTIC  SYMPTOMS  AND  TESTS 


("Evidence  ol 
neurotic 

I  tempera- 
ment.    No 

I  evidence  of 
Pain  iii  back,   organic 

1  disease. 


i  Evidence  ol 

organic 
disease. 

Pain,  tender- 
ness and 
rigidity  of 
spine. 


PAIN    I\ 
TRUNK  IN 
NERVOUS 

DISEASES. 


Girdle    pain 
(374). 


Pain  in 
thorax  and 

abdomen. 


(Tain  and  tender- 
ness of  spinous  pro- 
I  cesses. 

Pain    and    tender- 
I  ness  of  coccyx. 


May  follow 
traumatism. 


""Vertebral  column  is 
ankylosed 


Unilateral. 


Bilateral  usually. 


Plmli'as  ami  nervous  exhaustion,   pain  and  sen-e  i if  pressure   most    in 

Hysterical  symptoms  (426).     Much  tenderness  of  spinous  processes, 

Severe  pain  in  coccyx  without  evidence  of  any  disease  of  it.      Pain  ii 
symptoms  i4'2.">)  are  present. 


Severe  and  constant   pain  in  back  and  radiating  about   body  and 

Much  spasm  of  spinal  muscles.      Exaggerated  reflexes.      Little  or  i 
if  any,  it   is  of  a   transitory  nature.      Ilyperes  hesi.i   and   hyporalge- 


Slowly  increasing  motor  and  sensory  symptoms,  irritative  and  parah 
.       paralytic  symptoms  are  more;  prominent,  the  tumor  is  in  the  cord 
'       and  pain  radiating  into  extremities  than  in  meningitis  usually. 

It   may  lie  possible  to  feel  exostoses  on  vertebrae.     Unilateral  or  bib 

other  parts  of  the  body.      X-ray  examination  makes  the  diagnosis  | 


Pain  shoots  around  chest,  following  the  course 
nerve,  or  may  be  limited  to  a  small  area  of  the 

pericarditis,  pneumonia,  pleurodynia,  periost 

been  excluded  by  a  careful  examination. 


.Many   other  symp- 
|  toms. 


No      other      s; 
toms. 

\t  tn-st  unilateral  and  later  bilateral. 


Loss   of   knee-jerk. 
lit  if  infection. 


Argyll-Robertson's  phenon 


Mill. 


Ill  mamillary 
gland. 


In  precordia  and 


Along  attachment 

of  diaphragm. 


In  abdomen.  In 
all  these  rare  forms 
of  neuralgia  organic 
abdominal  disease' 
must  be  carefully 
and  thoroughly 
excluded, 


I  is  sterical 
toms. 

rOld  age, 

disease. 


Sj  lllp- 
Aiterial 


\n>  age.    No  arter- 
ial disease. 


In  genitals. 


There  is  a  zone  of  hyperesthesia  where  the  gir 

severe. 
History   or  other  evidence  of  syphilis,      l.umba 
Slowly  increasing  motor  and  sensory  symptoms 

Paroxysmal  attack-  of  pain  in  one  mammary  g 

can  be  detected.      Pain  is  usually  in  the  left    I 

Paroxysmal  attacks  of  pain  in  precordia  shooti 
region,  of  sulTocation  and  impending  death. 

Pain  similar  to  the  above,   but    QO  arterial  disea 
tobaCCO,  overwork,   etc. 

Pain    felt    in   lower  anterior  part    of  chest,   also  in  same  side  of  neck 
'render  points  are  along  the  attachment    of   the    diaphragm   and  bel 
t rouiely    rare  disease. 

'Paroxysmal   attacks  of  pain   in  epigastrium  often  occurring  at    the  sa 
ach    or   neighboring   viscera,   especially    no   gall  stones.      May  be  BBS 

Similar  paroxysmal    attacks  of  severe  pain,  occurring  irregularly  at  p 

Paroxysmal  attacks  of  severe   pain   in   abdomen   occurring  with  some 
Pain    relieved   by   pressure.      Blue   line  on   edge  of  villus,    wrist-drop 

Pain   in  hip,   groin,   liypogaslrium  and  genitals.      Tender  points  near 

Neuralgic   pains  and   irritability  in   the  pelvic  viscera,    the  bladder,   rec 
pains   at    limes  occur  during  years  in  one  testicle  or  one   labium   n 


OSTIC  ANALYSIS  OF  SYMPTOMS 

PAIN  IN  TRUNK 

0STRACT  OF  SYMPTOMS  DIAGNOSIS 

■d  in  cervical  spine  ;ui'l  occiput.  Neurasthenia  (1072).                 970 

aeially  in  mid-dorsal  region;  ovari le -   8  also  common  "vJotT'     ^"^    S"mihrA    "71 

Bed  '>•    motion,  touch,  defecation',  etc.     In  most  cases  there  is  a  history  of  injury.    Often  hysterica]  Cocoygodynia.                           >»72 

(Injury.    Very  sudden  onset.     Lumbar  puncture  maj   show  bloody  fluid.     Retention  Hematorrhaohis  (524).               973 

exIiemilH  -  "I    urine. 

History  of  infection    septic,  syphilis    etc.  .     Lumbar  puncture  shows  globulin  and  M'-"'"K''^  si""^'r.  "'/';'  ]-    ""» 

men,, lellular  elements  m  cerebrospinal  fluid,  gj  p^V    '"""'  ( 

[paraplegia  dolorosa).    When  irritative  symptoms  are  very  prominent  the  tumor  is  meningeal,  when  Spinal     Tumor     (509,     S-'ti.    976 

-tupt. nii~  .it  first  usually  unilateral,  later  bilateral.     Less  pain  and  spasm  in  back,  more  girdle  pain  836-40,  981,  1006). 

2 1-7. I 

'il  girdle  pains  at  level  of  thi    disease.     Rarely  any  paralytia  symptoms.     Usually  bone  lesions  in  Spondylitis    Deformans.     978 

we.  Arthritis  1  leformans, 

(Tender  points  of  Valleix:  one,  two  inches  from  posterior  median  line;  another,  two  [nteroostal  Neuralgia.                 977 
ii  intercostal          inches  from  anterior  median  line;  and  a  third,  in  mid-axillary  line,     Other  points 
■vc;  pleurisy,         on   nerve   may   also  be   hyperalgesia     Pain   is   paroxysmal.     Respiration,   cough, 
having          sneezing,  etc     lire  painful. 

Rash  "t  herpetic  vesicles  along  course  of  nerve.  Herpetic  Neuritis  (940  .             978 

n.     Lumbar  puncture  gives  lymphocytosis.     Uaoria.     Lightning  pains  in   legs,     History  of  syphi-  Tabes  (827, 661       (Fig  27        979 

in, I  below  a  bilateral  anesthesia,  which  may  !»■  Blight,  and  a  motor  paralysis,  which  may  be  Transverse    Myelitis       Figs     980 

J  17 

gtcture  gives  lymphocytosis.     Pains  worse  at  night.  Syphilitic  Meningitis,               980a 

first  irritative,  Liter  paralytic,     Brown-Sequard'e  paralysis  at  first   (442),  Spinal  Tumor  (976                     981 

I,  iiikI,  al  times,  radiating  beyond  the  l ts  of  the  breast.     No  tumoi  oi  other  disease  of  the  gland  Mastodynia,                               982 

■  to  left  ihoulder  and  even  down  left  arm  and.  at  times,  both  arms      Sense  of  oppression  in  Bternal  UigiiMrPectoris. 

■rial  ti  lee, ii  ,-  usimlh  high      \ie  i  ol  cardiac  dulneas  usually  increased 

Neurotic  nilivelu.il  who  has   ivn   overstrained   heart,      \t   tunes  the  result   of  gastric   indigestion,  Pseudo-Angina-Pectoi                 984 

t  frequently  on  left  side,     lircuthing,  sneezing,  coughing,  etc.,  painful.     Pain  Phrenic  Neuralgia,                     980 
:  mIitmi .-,l.-i, |, i  mi  i . .i, i   muscle      No  sign    of  pulmonarj    pleural,  cardiac  or  othi                     In  ex- 

ill>  in  tin-  e:nl\  iiinriiiiig.     No  diKeshve  disturbance*  or  evidence  of  urn  disease  of  atom-  Gaatralgia.                                   986 

Ii  cont  met  ion  of  il mpty  stomach  and  consequent  feeling  of  hunger. 

eck  of  bladdei                      uciated  with  symptoms  of  tabe     861  987 

odicity,  when  biliary,  renal  mid  other  forms  of  colic    appendicitis,  diverticuUti  i,  etc  have  been  excluded  Enteralgi  i     Lead  Coli     eti         986 
id  in  mine  nfter  administration  ol  l\    I 

ie,  on  en  il  i.i  ilium,  inner  pun  of  groin,  etc  Lumbo-abdominal  Neuralf 

i,  (torus,  vagina  and  urethra,  but  these  an  rare  and  relatively  unimportant  conditions      Neuralgic  Pelvic  Neuralgia.                       990 

mi  i  ti i-  pomi   the  pain  may  radi 


CHART  XV  c 

Pain  in   Extremities 


i  !omprising  Numbers  936  on  lefi  side  of  <  lharl 
and  905  to  1012  on  right  margin 


181 


DIAGNOSTIC  SYMPTOMS  AND  TESTS 
."  1  *;i i ii  iii  arm. 


Pain  limited  to  the 
trunk  and  distribu- 
tion of  the  sciatic, 
anterior    crural    or 
["Unilateral.    Any  of      obturator  nerve, 
these  forms  of  neu- 
ritis nia\    be  asso- 
ciated with,  or  pre-   ■', 
cede,    or    foDow    a 
rash  "i  herpes:  her- 
petic neuritis.  Pain  limited  to 
I  ige   :;:;.  38  .              outer  surface  of 
thigh. 


936 

PAIN  IN 
EXTREMITIES 
!\  NERVOl  - 
DISEASES. 


Pain  in  a  joint. 


Pain  at  insertion  of 
Achilles  tendon. 


Pain  in  heel 
I  Pain  in  toe. 


Willi    girdle    pains. 

and   lumbar  punc- 
ture gives 
lymphocytosis. 


\\  nh  am 


Bilati 


\\  nh  dissociation 
..I  sensation. 


\\  it  Ii  vaso-motoi 
disturbances 


DIAGNOSTIC  ANA 


ABSTRACT 


With  fat 


Pain  radiates  along  one  or  all  of  the  nerves  of  the  arm.  Te 
other  points  where  nerves  are  superficial.  Vaso-motor  di 
paralysis;  hut  movements  of  arm  are  impaired  by  the  pain 

pressure  on  nerves    must    he  carefully  excluded. 

Pain  shooting  along  the  trunk,  or  over  small  areas  ill  tin'  dish 
but  the  pain  may  prevent   motion.     Patient   holds  knee  of 

the  opposiie  side  and  bears  his  weight  on  the  healthy  leg. 
major  i  trochanteric  point)  and  in  popliteal  space  (popntea 
may  be  decided  muscular  weakness  and  atrophy.      Sciatica 
tinn  for  any  possible  pressure  upon  the  nerve  should  al\\a> 

Pain  along  the  trunk  and  distribution  of  the  anterior  crural 

ankle.  Tender  points  on  anterior  aspect  of  the  hip  joint, 
paralysed  and  atrophied  and  knee-jerk  lost  and  anesthesia  i 
be  secondary  to  diabetes  and  injury.     There  may  he  an  en 

Pain  along  inner  side  of  thigh,  along  course  of  obturator  ner 

..    neuralgia  and  is  usually  associated  will'  paralysis  of  the  ai 

Pain  is  assoeiated  with  paresthesia!'  (['specially  uumbiie--  an. 
The  paresthesia!'  are  more  characteristic  of  this  di-< 

Pain  in  a  joint,  usually  the  knee-joint,   increased  on  motion. 

dence  of  any  disease  of  tic  joint.    Many  hysterica]  symp 
Severe  pain  at  insertion  of  Achilles'  tendon  on  walking  and 

Pain  m  lower  surface  of  heel,  especially  when  walking 

removal  of  the  sub-calcaneal  bursa,  or  of  exostoses,  others 

Pain  in  the  nietatarso-phalangcal  joint,  especially  of  the  fourl 
is  lowered  from  "breaking"  of  the  arch  transversely. 

I  With  Romberg's  symptom,  ArgyhVRobertson's  phenomenon, 
J     lymphocytosis  and  lightning  pains  over  am  ill 

With  pain  ami  rigidity  in  back  and  in  extremities.     Exaggei 

("Steadily  progressive  motor  ami  Bensorj  symptoms,  al  first  mi 
Brown-Sequard's,  paralysis  (442). 

Motor  paralysis  and  anesthesia  over  whole  of  both  legs,  exci 
•J     peripheral  and  organic  reflexes.     Muscular  atrophy  and  ti 
m  lower  back  and  radiating  into  legs- 
Motor  and  sensory  paralysis  commencing  at  the  distal  end  i 
1     and  tenderness.    The  disease  usually  commences  with  pah 

Pain  and  parest  hoMae,  analgesia  and  thermic  anesthesia  wit 
symptom-  are  usually  limited  to  arms  with  symptoms  of  s] 
ire  milder 

Extreme  pain  in  soles  oi  feel  associated  with  redness  and  swell 
foot  must  be  excluded 

Pallor  and  coldness  of  fingers  and  toes  followed  l>y  cyanosis 
In  extreme  cases  a  larger  or  smaller  slough  forms  as 

Marked  Increase  in  fat,  either  diffuse  or  in  separate   tumors 
with  it.  and  the  fatts  masses  are  tender,  especially  in 


SIS  OF  SYMPTOMS 

TREMITIES 
SYMPTOM.-  DIAGNOSIS 

H  supra-clavicular  fossa,  in  axilla  a)  head  ol  radius  and  at      Cervico-brachial   Neuralgia  or   Neuritis  of   Dinar,      00.5 

■anees.     Fibrillar]  contractions  :i'  timi scur.     There  is  no  motor  Median  Radial,  etc 

"uuiors  at  base  of  neck  :ni'i  in  axilla,  and  a  ■<t\-k:iI  ril>    556),  causing 

[on  of  the  sciatic  nerve.    Little,  if  any,  anesthesia  or  motor  paralysis,      Sciatica    720  996 

ted  side  semi-flexed,  thigh  slightly  abducted,  inclines  lii>  body  to 
id.T  points  over  the  sciatic  notch    gluteal  point  .  above  the  trochanl 
lint  .     In  neuritis,  the  nerve,  wherever  felt,  is  tender,  and  then  there 
much  more  frequently  a  neuritis  tluui  a  neuralgia.     A  rectal  examina- 
I  made. 

,•<■  .hi  the  anterior  surface  of  the  thigh  and  inner  surface  of  leg  to  the      Crural  Neuralgia  or  Neuritis.  997 

it  side  ol  knee  tnd  at  internal  malleolus.  Extensors  of  thigh  maj  be 
be  mi  anterior  surface  of  thigh  and  inner  side  of  li'ii  in  neuritis.  May 
on  nf  herpes  along  the irse  of  the  nerve. 

after  hernia  and  other  diseases  have  been  excluded.      A  rare  form  of      Obturator  Neui  998 

(tors. 

iclnmi  and  is  frequently  associated  with,  and  is  caused  by,  flat  foot       Meralgu  Paresthetica  999 

the  pain,  which  i-  often  entirely  absent. 

In-  »kin  i-  much  more  sensitive  than  the  articular  surfaces.     No  evi-      Arthralgia  or  SystericaJ  Joint  1000 

-    I.'.", 

dmu.     Maj  follow  gonorrhea,  malaria,  gout,  broken  arches  or  injury.      AohiJlodynia  1001 

leumatic  medicine   other-  i>\  Burgical      Talagia  or  Calcanodynia.  1002 

supporting  'he  weakened  arches, 

lally  following  an  injury.     Usually  occurs  in  women.      I  "he  joint       Metatarsalgia  or  Morton's  rot  1003 

tory  of  syphilis  usually,  always  loss  ol  knee-jerk,  cerebro-epinal      Tabes      Neuralgic  stage   661  "Nil 

terficial  and  deep  often  followed  by  hyperalgesia  over  same 

\,.  ,i.i\ii      No  Irgyll-Robertson's  phenomenon,  Spinal  Meningitis   608  974  1005 

■  unilateral,  later  bilateral      Increased  pressure  ol  cerebro-epinal  fluid       Spinal  rumor   509,  826,  836-40,  976J  i|HN' 

the  domain  of  the  anterior  crural  nerve-      Abolition  ol       Lesions  ol  I  auda  Equina    187        Fig  -"'  1007 

.  i. -He -i,i  iii  perineum  and  genitals  and  much  pain 

tremitii  -   mil  extending  towards  bodv      Muscular  weaki atrophy      Multiple  Neuritis    iss  1008 

■  ml  fingers  and  often  with  fever 

iio|ilne  disturbances  and  mutilati  Syringomyelia  1150a,  1 1 7< •.  11^7.     1009 

i  be  pains  often  resemble  the  pains  of  tabes,  but  1357-9 

in, I  luter  with  pallor,  shrinking  and  wrinkling  ol  thesame  parts      I  lit       Erythromelagjs    1198  1010 

Congest  •  i lt ■  i  -   i'i-i  toes  i",  'I urplish  m,|  even  black       Raynaud's  Disease    1195  l'Mi 

in-  ml  lenH.  but  ti"i  elsewh  pain  tasooiated       \<lin"*i-  Dolorosa      Dareum  i  Dii  1012 

,  ih.  \    ir.  forming 


CHART   XV  d 

Vertigo 

i  lompriaing  Numbers  932  on  lefl  aide  of  <  !harl 
and  10l">  to  L033  on  right  margin 


DIAGNOSTIC  SYMPTOMS   wi>   I  i:sts 
Motoi   Uaxia  is  present. 


Cerebellar  Ataxia  is  present. 


932 
V 

]•: 

R 

T 
I 

G 

o 

(392 


I  irossed  Paralysis. 


\  ertigo  ;iinl  aun  emcnt  ol  head 


Deafness  and  symptoms  of  aural  dis 


Diplopia  and  symptoms  of  ocular  disease 


Position  and 
moving. 


Symptoms  "I 

circulatory 

disturbances 


Digestive  dii 
orders. 


( '.-inline  and  hen 
disease. 


\i  herqmatous 
arteries. 


1 1  i  k  h  blood 
tension. 


Apoplexy. 
Epileps; 

Migr: 


Toxic 


Organic 


Symptoms  ol 
cerebral  di 

,  te 


Functional. 


DIAGNOSTIC  AN 


DISORDERS  OF  SENSAT 
A.BSTB  \*    i 

In  these  cases  the  vertigo  is  not  a  prominent  symptom.     In  - 

of  falling  and  fears  that  he  will  fall  and  experiences  some  vert 
lesions  in  the  brain  stem  and  el  en  here.     The  diagnosis  is  made 

\n\  disease  of  the  cerebellum,  especially  tumors,  max  cause  vertig 
tin1  hemispheres.     The  di  >m  I  hi    absence  of  p 

and,    III  III 'S,  the  Optic   lnairil  is  ami    failUTI     Ol 

Lesions  of  the  brain  stem  may  involve  the  tracts  From  the  cerebell 
made  by  the  motor  or  sensory  paralysis  or  both,  which  occur  it 
paralysis  in  the  domain  of  the  cranial  nerves  (crossed  paralysis 

Cysts  and  tumors  suspended  free  in  the  fourth  ventricle  cause  in1 
the  diagnosis  is  extremely  difficult  or  impossible.  The  vertigo  i 
held,    i  Ihoked  disc  is  common, 

\  steadily,  progressive  deafness  of  one  ear  associated  with  tinnitt 
may  throw  patient  in  the  ground.  Raising  the  head  from  the  | 
or  loss  nf  bone  conduction  and  loss  of  power  of  hearing  high  m 
theparoxj   mal  attacks.     Suppurative  and  other  diseases  of  the 

the  ear  is  completely  deal',  but  then  may  commence  in  tl th 

cause   vertigo   by   affecting    the   semi-circular   canals   or   vesl 
laesa).     It  is  difficult  to  draw  the  line  between  these  case 
all  these  conditions.     Strictly  speaking,  Meniere'    disease  appl 
Bammation  of  the  labyrinth  causing  vertigo  is  called  Voltonrs 

Double  vision  and  weakness  of  ocular  muscles  and  ■  ■■  strain  ma; 
is  relieved  by  closing  the  defective  eye,  even  when  it  is  not  cau 

When  patient's  head  is  bent  down  for  a  I  id  then  is  sudd 

vertigo      A  blovi  on  the  head  will  cause  vertigo,  prol 

back  of  head  or  moving  head  quickly  may  cause  vertigo.      A  B\ 
to  the  head. 

Great  weakness,  especially  in  the  convalescence  from  disea 

When,  in  consequence  of  the  congestion  due  to  digestive  di 
are  anemic.     These  digestive  disorders  ma\  also  produce  abno 
diagnosis  is  made  by  the  presence  of  the  digestive  disorder  and  1 

In  all  inn  us  of  cardiac  disease  the  brain  maj  receive  an  insufficien 
frequent  in  aortic  disease.  The  diagnosis  is  made  From  the  pn 
to  the  altered  quality  than  quantity  of  the  blood  supply   i  1029 

Atheromatous  arteries  interfere  with  the  normal  bl 1  supply  bot 

cause  vertigo.     This  is  especially  common  in  elderly  people.     T 
usually,  an  increased  artei  ial  tension. 

Fulness    of    head,    headache,    mental    confusion,   tinnitus  auriui 

tension. 
Vertigo  is  a  common  initial  symptom  of  apoplexy  of  all  form     ■  ■ 

rhage)  and  may  be  the  only  .symptom  of  a  slight  attack.      Isua 

Vertigo  may  constitute  the  aura  which  may  or  may  no!  be  Follow© 
In  some  cases  a  severe  subjective  sensation  of  vertigo,  frequently 
Vertigo  is  a  not  uncommon  symptom  in  the  interval  between  tl 

Vertigo  may  be  the  initial  symptom  or  may  accompany  an  attaol 
mal  es  the  diagnosis  plain, 

Abnormal  conditions  of  the  bl I,  as  in  the  early  stages  of  the  in 

Various  toxic  substances,  such  as  tobacco,  alcohol,  coffee,  morphia, 

of  the  cerebral  or  cerebellar  cortex.    The  diagnosis  is  made  by  thi 

\  di-ea  e  endemic  in  Switzerland  and  occurrii nJ     n  war! 

ness  of  vision,  ptosis,  often  diplopia  without  strabismus,  and  a 
Pain  in  back  of  neck,     attack  lasts  a  fen  minutes. 

In  addition  h    apoplexy,  any  irritation  of  the  meninges  itumorsji 

oiated  with  tevere  vertigo,  especially  on  change  of  position.     Ti 

pressure  on   I  he  CI  n  bl  Hum,  or,  il ated    in    the  frontal  lul 

oade  by  the  numerous  other  symptom    of  these  di  ea 

with  the  vertigo,   which   is  less  severe  in  the  recumbent    posture 

Vertigo  is  a  not  uncommon  symptom  in  those  functional  nervous  • 
in  h  i-  neurasthenia,  the  traumatic  neuroses  and  hysteria.     Thi 

VerUgO  is  never  very  severe  and  often  resembles  rather  syncop: 


YSIS  OF  SYMPTOMS 


••I;  PERVERSION:    VERTIGO 
d    SYMPTOMS 

■s.  in  consequence  of  the  incoordination,  the  patient  is  in  danger 
while  in  other  cases  the  vertigo  may  be  the  direct  result  of  the 
m  the  presence  of  motor  ataxia. 

Iiirh  is  more  permanent  in  lesions  of  the  vermis  than  in  those  ol 
pis,  the  presence  of  cerebellar  ataxia,  headache,  and  vomiting 


DIAGNOSIS 
Tabes,    Disseminated   Sclerosis  and  other  disease    1015 

with  ataxia. 


Cerebellar  Disease  (609-10,  648,  686,  7s:;.   1272).     loin 


Bid  cause  ataxia  and,  less  frequently,  vertigo.    The  diagnosis  is 
,e  form  of  hemiplegia  with  increased  reflexes,  and  also  of  local 

D  .       Fig      19-22.) 

Dizziness  only  when  head  is  moved.     Except  for  this  symptom 
vary  greatly   in  intensity  with  the  position  in  which  the  head  is 


Lesions  of  the  brain  Btem     WO,  535-46,656,830,     1017 
L268-74,  1301-4,  L375,  1378,  1382-4,  1388,  i:J98). 


Lesions  within  the  fourth    ventricle.     (Kg,  19.)      101s 


1  that  ear,  and  with  paroxysmal  attacks  of  severe  vertigo  which 
r,d  may  cau-e  vomiting.  \t tacks  vary  in  severity.  Impairment 
ure  usually  present.     Vertigo  1-  usually  entirely  absent  between 

may  be  present    but  usually  arc  not.    Disease  usually  ceases  when 

I-.     \im  1  e  01  functional  disturbance  of  the  ear  may 

ir   nerve   directly  or  indirectly  (aural  vertigo  or  vertigo  ab  aure 

vertigo  ami  Meniere's  disease,  which  latter  is  often  used  to  cover 

:    ge  into  the  semi-circular  canals.    In- 


Meuiere's      Disease.        Voltoni's      Disease  \ural 

Vertigo.     Vertigo  ab  aure  laesa  (650,  685,918)      1019 


li  BUI         imetimes  on  railway   trains 
by  tin-  diplopia  alone. 


■used,  or  when  patient's  body  is  rotated  rapidly,  he  experiences 

ol  vaso-motor  reflex  disturbance.     Lying  on  one  side  of 

tcvertigo  rom  the  application  of   1  galvanic  current 


rhe  vertigo      Ocular  Vertigo.     Vertigo  ah  oculo  laeso  (649).        1020 
\cute  ( lerebral  Anemia  1021 


niiili  cause  lioth  of  vertigo  and  ataxia. 


Exhaustion  Vertigo 


he  portal  circulation   is  engorged  with  blood,   the  cerebral  vessels        Acute   Cerebral    Anemia    from    digestive    disorders       1023 

I  chemical  substances  which  may  produce  a  toxic  vertigo.    The  hemorrhage,  etc 

vertigo  when  the  indigestion  i-  cured. 


-I  irregular  supply  of  1.1 1  and  vertigo  may  result.    Tin-  i-  most 

in  hemic  diseases  the  vertigo  is  due  rather 


(  'lironic   ( 'erebral    Anemia    I  n  >m 

diseases. 


ilood  and  cardiac 


io  uniformity  of  distribution  anil  hence  ma\  ('lironic  ('erebral    \nemia  from  atheromatous  alter-      1025 

m  de  from  the  pr<  »encc  ol  atheromatous  arteries  with,  ies  (syphilis 

palpitation  of   heart,   dyspi a   on    exertion,    ami    high    blood  Cerebral  Congestion 

I  hemorrhage,  embolism  and   thrombosis,   and    meningeal  hemor-  kpoplexy  (504). 

i.  :n 

i  full  attack.     The  diagnosis  is  made  from  the  ep                   cks  Epilepsy  (575,  1058,  1071 
il  iwed  bv  vomiting,  maj  he  the  equivalent  of  an  epileptic  attack. 
ntinuc  durum  mmute-  or  hours. 

migraine.     The  hemicrania,  th<  much  more  prominent  symptom,  Migraine    B46,  854,  949 


mil  in  leukemia,  melanemia   gout,  diabetes,  etc. 


go    in.' I 


bablj  bj  affecting  the  circulation      Drug  Vertigo  1080 

ii  f  of  the  ingestion  ol  the  sub  of  vertigo. 

r  n  hot  ortigo,  with  dim       Gerliei     Vertigo     Vertige  Paral  1031 

■  ■  .i,  ..i  net  ..I  the  firms,  simulating  bj   I 

inflammation  Cerebral   Meningitis  and   Tumor    Syphilis      508,     i";-' 

ci  of  the  meiimce-  ami  h\    li  in   mitted 

b\  direi  tct       The  diagni 

iting,  dow  pul-e,  etc.,  which  aiv  frequently  a  sociated 


cute  and  chronic,       Neurasthenia,    rmumntic   Nei 

'  !..■!  .  hart        I  in-  101 


CHART  XVI 

Disorders  of  Cerebral  Activity 


DIAGNOSTIC  ANALYSIS  OF  SYMPTOMS 

Symptoms  Alterations  in 

Analysed  Mentality 

'1037 

Coma.  See  Chart  XVI  a. 


1036 

Disordered  Mentality. 


1038 
Pseudo-Coma. 

1039 

Double  Personality. 

1040 

Weakened  Mentality. 


1041 
.Insanity . 


"See  Chart  XVI  b. 


See  Chart  Wl  o. 


1H-, 


CHART  XVI  a 

Coma 

( Comprising  Numbers  L037  on  left  side  of  Chart 
and  1042  to  1068  <mi  right  margin 


1ST 


DIAGNOSTIC  SYMPTOMS  AND  TESTS 


•History,    or    other 
evideni 

injury  to  head. 


<  'onvulsions  rare. 


Pupils     usually    contracted    and 
respond  feebly  to  light . 


History  of  a  pre- 
vious brain  illness, 
of  which  the  coma 
is  only  one  symp- 
tom, and  often  the 
terminal  one,  or  the 
presence  of  an  in- 
flammation of  the 
scalp  (etyispelas, 
suppuration),  or  of 
thi'  bones  of  the 
skull  (caries  and 
especially  suppura- 
tion of  the  bones 
of  the  ear1. 


History  or  other 
evidence  of  poison- 
ing. 


Evidence  of  a  car- 
diac inadequacy. 


Sudden  attack  of 
corns  of  short  dura- 
tion with  or  with- 
out   a    convulsion. 

Usually    a    history 

of  similar  attacks 
an. I  often  of  remote 
injury. 


Sudden     attack    of 

unilateral  paralysis. 
Rarely  il"-  paraly- 
sis comes  on  slowly; 
steadily  increasing 
during  hours  or 
days,  "Ingraves- 
cent apoplexy."  In 
such  cases  the  coma 
may  be  slight  or 
absent 


Albumen  and  casts, 
or  sugar,  or  all 
three,  in  urine. 


u-ver.       1 

I 

rexia.      J 


Patient  may  be  completely  unconscii  | 
toms  follow  the  injury  immedi  I     I; 


Convulsions       are 
frequently  present. 


No  convulsions. 
Convulsions  rare. 


Convulsions  absent. 


Often  a  slight 
spasm    or    rigidity 
during  the  attack. 

( 'onvulsions  almost 
always  present  and 
are  usually  the 
most  si  liking 
symptom     of    the 
disease,  but   not   so 
characterist  ic  as 
unconsciousness, 
which isai  timesthe 
only    symptom    of 
i  lie  attack. 

Convulsions    are 

rare,  but  both  tonic 
and  clonic  spasms 
may  occur,  involv- 
ing one-half  of  I  lie 
body  when  the  le- 
sion is  cortical,  or 
involving  both 
sides  of  the  body 
when  the  hemor- 
rhage occurs  in  the 
brain  stem  (460)  or 
ruptures  into  a  ven- 
tricle. 


f  No  convulsions. 


1  Convulsions 
ally. 


Convulsions 
quently. 


fre- 


Pupils  dilated,  often  unequal,  and  Symptoms  usually  follow  the  injury 
usually  do  not   respond  to  light.  symptoms.     Often  conjugate  devi: 

'The  symptoms  are  those  of  a  local  meningitis  (">07,  1045)  or  abscess  i/iOS, 
the  coma  are  common.  There  may  be  local  symptoms,  both  irritative  a 
be  edema  of  eyelids  and  conjunctivae,  choked  disc,  prominence  of  the  ey 

Retraction  of  neck  and  opisthotonus.  Fever,  headache,  delirium.  Convul 
tation  followed  by  those  of  paralysis. 

Headache,  vertigo  and  vomiting.  Often  mild  delirium.  A  recent,  infectei 
general  and  resemble  those  of  a  rapidly  growing  tumor.    Choked  disc 

Headache,  vertigo  and  vomiting.  May  be  a  history  of  former  injury.  No 
tumors  at  the  base  are  more  likely  to  cause  paralysis  of  one  or  more  ci 

A  motor  monoplegia  (anarthria,  etc.),  rare,  hemiplegia  or  diplegia  occurrii 
defect.     Epileptiform  convulsions,  unilateral  or  bilateral,  are  frequent. 

Progressive  mental  impairment,  childishness,  restlessness,  amiable  but  irri 
syllables  and  letters  are  left  out  and  letters  doubled.     Apoplectiform  an 

History  of  lead  poisoning,  of  lead  colic,  of  wrist-drop,  etc.    Blue  line  on  g 

Intention  tremor.     Scanning  speech.     Many  motor  and  sensory  symptom 

Headache,  increasing  fever,  difficulty  in  walk  and  speech,  tremor,  increasi 

Patient  can  usually  be  aroused  from  his  coma  sufficiently  to  speak  and  his 
alcoholic  abuse. 

Pupils  are  contracted  and  do  not  respond  to  light  (if  opium).  Patient  is 
other  narcotic. 

{  Patient  is  in  a  confined  space  or  room  in  which  there  is  a  strong  smell  of  il 

Sudden  attack  of  coma  with  pallor  and  weak  or  absent  cardiac  action  of  si 
extremities  cold,  restlessness,  yawning.     Low  arterial  tension,  steadily  g 

Sudden    intermission  of  heart  beat  during  a  considerable  fraction  of  a  mini 

'The  attack  usually  commences  with  a  convulsion,  as  described  in  Chart  X,  5 
sometimes  trivial,  sometimes  a  deed  of  violence  (post-epileplie  insanity) 
sciousness  and  no  convulsion  and  either  no  action  or  some  trivial  or  fool 
the  convulsive  attack  ami  is  called  the  "psychic  equivalent"  am!  is  altoj 
and  take  journeys  ami  are  lost  to  their  friends  and  to  I  hemselves.  After  a 
an  epileptic  attack  is  the  complete  or  almost  complete  unconsciousness  i 

some  mental  weakness  which  may  slowly  increase  to  mild  Or  extreme  de 
epileptics  have  attacks  during  many  years  ami  yet    show  little,  or  no,  I 

The  attack  is  altogether  similar  to  the  major  attack  of  epilepsy,  but  i 
distended  abdomen,  foul  smelling  feces,  vomiting,  diarrhoea,  etc.,  and 

Thecoma  comes  on  instantly  or  in  the  course  of  a  few  hours.  There  are  tert 
in  the  form  of  hemiplegia.  'The  bilaterally  innervated  muscles  (upper  fa 
ion-,  abdominal,  micl  tuition,  defecation,  etc.)  escape  permanent  paralysis. 

reflexes  may,  during  the  coma,  be  abolished,  later  exaggerated  (Rosenba 
pass  away  alter  several  hours  or  days.  The  lower  branch  only  of  the  fa 
i  he  paralysed  side.  Usually  there  is  also  at  first  a  sensory  hemiplegia  > 
in  which  latter  ease  the  motor  paralysis  greatly  improves  or  entirely  disi 
in  leg  and  finally  in  the  arm.  In  case  recovery  does  not  take  plai 
in  leg.  1'osl  hemiplegic  motor  disturbances  may  occur,  especially  in  h: 
toms  such  as  aphasia  may  occur.  A  reactive  inflammation  about  'he  lei 
second  week.     Repeated  attacks  at   varying  intervals  are  common. 

After  uncertain  prodromata,  coma  and  paralysis  with  fever  appear  and  de. 
.     encephalitis  superior  hemorrhagica  acuta)  or  may  be  in  the  form  of  a  he 

Patient  emaciated.    Acetone  odor  of  breath.     Pulse  is  email  and  rapid,  ski 

Onset  usually  gradual.  Some  edema,  cyanosis,  restlessness,  rapid  noisy  resj 
albumen  and  casts. 

'  Occurs  at  the  onset  of  acute  infections,  especially  in  children.  Often  associ 
hut  in  these  eases  convulsions  are  rare,  and  the  cause  may  consist  in  a  fa 

History  or  evidence  of  exposure  to  great  heat      Absence  of  perspiration. 
symptoms  (paralytic)  occasionally  occur 


DIAGNOSTIC  ANALYSIS  OF  SYMPTOMS 


ABSTRACT  OF  SYMPTOMS 


DIAGNOSIS 
Cerebral  Concussion. 


r  a  short  time  after  which  he  remains  in  a  dazed  condition  for  a  time,  or  he  may  be  only  dazed  from  the  start.  Pallor,  low  blood  tension,  vertigo  and  vomiting  are  common  symptoms.  May  be  contusion  of  scalp.  Symp- 
irely  any  paralysis.     Often  retrograde  amnesia  (769). 

jiately  but  not  always;  there  may  be  a  "lucid  interval,"  (especially  in  extra-dural  hemorrhage).  Coma,  profound  stertorous  breathing,  pulse  slow,  reflexes  abolished,  increased  tension  of  cerebro-spinal  fluid  are  the  usual 
)f  hea'd  and  eyes'     Often  paralysis  in  the  form  of  more  or  less  complete  hemiplegia,  together  with  Babinski  reflex  and  some  spasm.     Often  retrograde  amnesia  (769). 

)  with  usually  high  fever  and  chills  (both  may  be  absent)  occurring  in  a  cachectic,  anemic,  or  infected  patient,  especially  in  one  with  caries  of  bone  of  skull  (otitis).  Headache,  vomiting,  restlessness  and  delirium  preceding 
ralytic.  A  very  characteristic  symptom  is  a  localized  edema  of  the  scalp.  In  thrombosis  of  superior  longitudinal  sinus  there  may  be  epistaxis  and  edema  at  root  of  nose.  When  the  cavernous  sinus  is  involved  there  may 
ind  oculo-motor  and  abducens  paralysis.     When  the  transverse  sinus  is  involved  there  may  be  edema  over  mastoid  and  palpable  thrombosis  of  internal  jugular  vein  in  upper  part  of  neck. 

and  retraction  of  abdomen.    Paralysis  of  cranial  nerves.    Kernig's  reflex.     Lumbar  puncture  and  examination  of  the  fluid,  which  may  be  cloudy,  give  globulin  and  increased  cellular  elements  in  it.    Symptoms  of  cerebral  irri-        Meningitis,  (590,  608). 


Cerebral  Compression 

(contusion  and  hemorrhage). 

Sinus  Thrombosis,  (964). 


nd  or  other  cause,  or  origin,  for  suppuration.    Moderate,  irregular,  often  absent  fever.      Course  is  progressive  but  may  be  very  acute  or  extremely  chronic  and  often  shows  a  latent  period.     The  symptoms  are  both  local  and 
rather  rarely.     The  general  symptoms  are  more  prominent  than  the  local.    Suppuration  of  the  middle  ear  and  of  the  mastoid  cells  must  be  carefully  excluded,  especially  in  children  (see  508). 


Course  is  progressive.    Mental  deterioration,  but  local  sympto 
erves.    Choked  disc  is  very  common  (see  507,  897). 


often  as  prominent  as  the  general.     Convulsions,  especially  Jacksonian  epilepsy,  are  common,  especially  when  tumor  is 

muscular  atrophy,  and  reflexes  exaggerated.     Ankle-clonus  and  Ba 


or  near  the  cortex;   while 
ski.     Usually  some  mental 


genitally,  or  in  early  infancy  are  common.      Usually  some  arrest  of  development  of  paralysed  part  and  of  skull.     Little 
athetosis  and  hemichorea  frequently  complicate  the  disease  and  contractures  occur  in  almost  every  case. 

6teadily  increasing  dementia.    Blurred  speech.    Tremor  of  lips,  tongue  and  hands.     Terminal  dementia.     Inability  to  repeat  difficult  phrases,  due  partly  to  paraphasia,  partly  to  loss  of  memory.      Writing  imperfect:  words, 
vulsive  attacks.    Abnormalities  of  pupil.     Argyll-Robertson's  reflex.     Lumbar  puncture  gives  globulin  and  lymphocytosis  in  cerebro-spinal  fluid.     History  of  syphilis.     Positive  Wassermann  reaction. 

Convulsions.    Lead  can  be  found  in  the  urine,  especially  after  the  administration  of  K.  I. 

:aggerated  reflexes.     Ataxia.    Nystagmus.    The  convulsive  attacks  may  be  epileptiform,  apoplectiform  or  myotonic.     Headache,  compulsory  acts  and  slight  dementia  are  not  uncommon  symptoms. 

'Wsiness,  passing  into  coma  and  death.    Trypanosomes  are  found  in  blood  and  in  cerebro-spinal  fluid. 

i  is  characteristic  of  intoxication;  being  indistinct,  blurred  and  foolish.    Pupils  are  dilated  and  respond  to  light.    Flushed  face  and  conjunctiva,  and  stertorous  respiration.     Often  tremor  or  twitching.     History  or  evidence  of 


Cerebral  Abscess, 

(152,  181,  508,  578,  587,  907,  960). 

Cerebral  Tumor,  (151,  507,  536-42 
578,  5S7,  S33,  S49,  S55,  S5S,  861,892,  960). 

Cerebral  Palsy  of  Childhood. 

Porencephaly,  (116, 501, 577,  630,  798, 10S6). 


Paresis,  (1104). 

Lead  Palsy,  (158,  494,  584,  788). 
Disseminated  Sclerosis,  (668). 
Trypanosomiasis  or  African  Lethargy. 
Alcoholic  Coma,  (764). 


1049 

1 
1050 

1051 

1052 

1053 


*-sy,  and  mentally  incapable.     Respiration  is  slow  and  stertorous.    Face  is  congested.     Pulse  is  at  first  slow,  but  later,  especially  in  fatal  cases,  becomes  rapid.    History  or  evidence  of  patient's  having  taken   morphii 


Narcotism  from  opium,  etc. 


1054 


ating  or  coal  gas.    He  is  cyanotic  with  rapid,  irregular  pulse.     He  often  vomits   and   exhibits  more  or  less  tonic  or  clonic  spasm. 

uration.    Often  preceded  by  tinnitus  aurium,  dimness  of  vision,  cold  sweats,  and  nausea.    Slight  spasm  or  rigidity  is  frequent  during  the  attack.    In  internal  hemorrhage  the  onset  of  the  coma  is  more  gradual.    Pulse  is  small, 
g  lower. 

more  with  coma  and  slight  spasm.     Slow  pulse,  atheromatous  arteries.     Usually  occurs  in  advanced  age. 


^he  convulsion  lasts  only  two  or  three  minutes  and  is  accompanied  and  followed  by  a  com; 
.h  an  attack  of  general  convulsions  is  called  "the  major  attack"  or  "le  grand  mal."  At  til 
tion;  unconscious  movements  of  lips  and  jaws  being  common.  This  is  called  "the  minor 
to  the  post-epileptic  insanity.    These  attacks  may  last  minutes,  hours,  or  days 


which  gradually  passes  into  a  sleep.  This  post-epileptic  coma  is  sometimes  absent  and  is  sometimes  replaced  by  unconscious  action, 
res  such  an  attack  follows  another  immediately  throughout  a  long  series  (status  epilepticus).  At  other  times  there  is  only  uncon- 
attack"  or  "le  petit  mal."    Sometimes  the  attacks  occur  only  at  night  (nocturnal  epilepsy).    At  times  an  attack  of  insanity  replaces 

d  in  them  the  patients  lose  their  former  individuality.     In  some  of  these  attacks  (ambulatory  automatism)  the  patients  wander  about 

fks  there  is  amnesia.  A  rare  form  of  epilepsy  is  one  in  which  the  patient  falls  suddenly  to  the  ground  and  gets  up  again  immediately  without  any  appreciable  loss  of  consciousness  (vertiginous).  The  essential  characteristic  of 
il  and  the  complete  or  almost  complete  absence  of  any  memory  of  it.  In  the  interval  between  the  attacks,  which  at  times  extends  over  months  and  years,  the  patient  may  be  entirely  normal.  Frequently  he  is  irritable  and  shows 
:i,  especially  il  the  attacks  are  frequent  and  rest  on  a  strong  hereditary  basis.  This  condition  is  not  to  be  confounded  with  the  transitory  mental  impairment  due  to  bromide  given  therapeutically.  On  the  other  hand,  many 
I  impairment.     Epilepsy  beginning  in  a  patient  over  forty  years  of  age  should  suggest,  the  possibility  of  a  cerebral  tumor. 


Illuminating  or  coal  gas  poisoning. 
Syncope.     Internal  Hemorrhage. 

Stokes-Adams'  Disease,  (436,  582). 

Epilepsy,  (110,  126,  430,  575,  S46, 
1027,  1071,  10S3,  1102). 


ecur.    There  is  only  one  attack  or  a  series  of  attacks  at  short  intervals.     It  can  usually  be  referred  to  an  irritation  of  some  part  of  the  body  or  to  some  form  of  poisoning 
when  these  conditions  are  removed.     It  is  most  common  in  children. 


It  is  often 


:iated  with  digestive  disturbances,        Eclampsia,  (576). 


respiration  and  a  slow  full  pulse.  Usually  paralysis 
Jcular,  masticatory,  deglutition,  laryngeal,  respira- 
iski  reflex  usually  present  from  the  start.  The  other 
ign).     Patient  may  die  in  coma  or  the  coma  may 

decidedly  paralysed.  Tongue  protruded  towards 
quickly  disappears,  but  which  may  be  permanent, 
rs.  Improvement  usually  begins  in  the  face,  next 
itraetures  appear  in  arm  and  extensor  contractures 

Some  mental  impairment  persists.  Local  symp- 
ray  cause  an  exacerbation  of  the  symptoms  in  the 


d  later  in  disease.     Hemiplegia  disappears  quickly 
ted  with  cerebral  miliary  aneurisms).    Permanent,  or 


Prodromal  symptoms  (headache,  vertigo,  etc.)  common.     Convulsions,  especially  Jacksonian  epilepsy  (431),  at  onset 
and  completely. 

Prodromal  symptoms  may  or  may  not  be  present.     Profound  and  long  coma  usually.     High  arterial  tension  (: 
long  continued  hemiplegia.     Aged  patient.     Presence  of  interstitial  nephritis. 

No  prodromata.  Youthful  patient.  Cardiac  or  pulmonary  disease,  sepsis  or  aneurism.  Existence  of  embolism  elsewhere  in  body.  Slight  or  absent  coma.  Pulse  not  so 
slow.    Hemiplegia  not  so  permanent.    Paralysis  of  some  cortical  function;  aphasia,  hemianopia,  etc.     Spasms  not  infrequent. 

Prodromal  symptoms  present.  Slight  or  no  coma.  Atheromatous  arteries  or  history  of  syphilis.  Paralysis  of  some  cortical  function;  aphasia,  hemianopia,  etc.  A  mild, 
transitory  form,  with  tendency  to  relapses  and  without  contracture,  is  the  so-called  "lacunar  hemiplegia,"  in  which  not  one  large  focus,  but  numerous  minute  foci  of 
softening  occur  in  the  cortical  area  involved. 


Pachymeningitis  Interna  Hemorrhagica, 
(502,  5SS). 


Cereln-al  Hemorrhage, 

(146,  411-13,  503,  58S,  832,  856-7). 


Cerebral  Embolism,  (505,  832). 
Cerebral  Thrombosis,  (506,  832,  1207). 


asulti 

gia,  partial 


two  or  three  weeks.    The  disease  usually  occurs  in  young  persons  and  seems  to  be  due  to  poisoning,  especially  alcoholii 
1  "-  complete. 


Optic  neuritis  may  be  present.     The  paraly 

Breathing  is  labored  and  may  show  "air  hunger."    Sugar  and  almost  always  albumen  and  casts  also  in  urine. 
Pulse  of  high  tension.    History  usually  of  headache,  vomiting,  dyspnoea  and  dimness  of  vision.     Ophthalmoscope  may  show  albuminuric  retinitis.    In  ra 


may  attack  the  eye  muscles  (Wernicke's  polit 


tinitis.    In  rare  cases  there  may  be  hemiplegia  or  other  paralysis.    Urine  contains 
"circuhtion  Tcereebra°nan  'n'  f?U'  smelling  feceSl    High  fever  is  common.    Often  history  of  improper  food.    The  coma  which  occurs  in  the  course  of,  and  especially  towards  the  end  of,  acute  infectious  fevers  is  probably  of  this  nature, 


.  comes  on  rapidly  but  not  instantaneously  and  is  preceded  by  many  prodromata;  such  as  headache,  mental  confusion,  marked  disturbances  of  vision,  paresthesiae,  weakness,  etc.     Delit 


symptom.    Local 


Diabetic  Coma. 

Uremic  Coma,  (576,  581,  850,  956) 

Toxic  or  Auto-Toxic  Coma,  (596). 

Sunstroke  or  Insolation,  (589,  966). 


1055 
1056 

1057 
1058 


1059 
10  50 
1061 
1062 
1063 


Acute  Multiple  Encephalitis,  (495,  543-4).  1064 


1065 
106P 

1067 

100S 


CHART  XVI  b 

Pseudo-coma,  Double  Personality  and  Weakened 

Mentality 

( lomprising  Numbers  10:iS  to  1040  on  left  side  of  <  Iharl 
and  1069  in  l()7.">  on  ri^ht  margin 


IS'.t 


1038 

PSE1  I  id-COMA. 


HI  AGNOSTIC  SYMPTOMS  AND  TESTS 

Hysterica]  symp- 
toms (425). 


/-Hysterica]  symp-     ' 

loins  i  125). 


DOU  BLB  PERSONALITY  .VXD  AUTO- 
M  \  II  sm   (209). 


Epileptic  symp 
Items  (575). 


( lonvulsiona  and 
Spasms  frequent. 


( ionvulsions 
frequent. 


DIAGNOSTIC  ANA  f 


PSEUDO-COMA,  DOUBLE  PERSON 

\BSTK.\CT 

Occurs  usually  in  girls  and  women  ol  an  emotional 
be  stopped  by  a  strong  and  continued  pressure  o 

vation  will  usually  show  that  she  is  attentive  to 
from  external  causes,  or  auto-suggestion  ihypnoti 

("Patient  seems  a1  tunes  to  be  in  a  hypnotic  .stall-.  09 
ami  in  that  stall-  lo  lead  a  life  carried  on  from  6 
states  from  auto-suggestion,  patients  often  act  like 
tion  and  in  some  hysterica]  patients  max  well  In-  .I 


While  in  an  unconscious  state  patient  often  perform 

has  no  memory.      Whether  in  such  unconscious  st 
doubtful.     While  unconscious,  epileptics  often  pel 


Apprehension    and    various    phobias   are 

prominent  symptoms.     In  consequence 

of  ^flidjr1 /v'e\*ene3^  OnJktiljJ  ""these 

f     panwm  cun^yt  rid^lrcm^l+eA.Ajy^rea- 

soning,     of    their   unreasonable   appre- 

bans^E^W  bdii  /jflurioH-rctS  alduoG 


^ilfrtnaM 


licil'J  lo 


1040 

WEAKENED  MENTALITY.  Patients 
appear  to  be  intelhgent,  but  incapable 
of  king  sustained  effort,  and  of  self- 
control,  often  foolish  and  unreasonable 
The  different  diseases  in  these  groups 
merge  into  each  other  and  no  sharp 

line     can      be     drawn      between      them. 
They    all   rest    on    a    neurasthenic    basis, 

-ml    in    all    suggestion    plays    a    greai 
part. 


twj*  kwmhirxci  u  yijrjtiicj,  i )  nwjipMtbk 

ana  incredible.     No  certain  evidence  ot 

any  organic  disease;  although  almost 
every  disease  can  be  more  or  less  per- 
fectly simulated  (425). 


The  symptoms  are  those  of  a  general  exhau 

especially  of  the  lower  centers.     It  is  common  in 

easily.     Every  task  looms  as  a  mountain  before  I 
will  power  are  both  poor.     They  feel  nervous,  ir 
phobia,  claustrophobia,   etc.  I.      Almost    as  eharacl 
The  patient  also  suffers  much  from  palpitation, 
five  disturbances.     The  essentia]  symptoms  of  m 

The  patient,  usually  a  male,  is  in  a  condition  of  exfa 
consciousness  in  which  the  attention  is  firmly  and 

pressed  because  of  a  delusion  in  regard  to  a  suppo 

fi!f'Winrhi*fiFl?Ir'WP™i  abnormal  .sensations.  I 
'JM-VV,uf  the  rjaWMea  Cannot  be  dispelled  from 
strous,  fantastic  and  impossible.  At  times  they  S 
and  apprehensive,  and  their  attention  is  firmly  li 
even  grotesque  delusion  that  some  organ  of  the  l> 

.The  disease  occurs  almost  exclusively  in  women  and 
M1  ^H#<Mri,'  are  probably  all  really  cerebral  and  seem 
adopted  by  the  patient   as  the  reSllH   of  imp 
patients  are  usually  so  dominated  by  the  desire  t' 

of  accomplishing  this.    Too  much  reliance  cannot, 

stimuli  varies  from  day  to  day  and  is  often  quite  I 
(425).  Anesthesiae,  paresthesiae,  hypcresthesiae. 
disturbances  occur  alone  or  combined,  transitory  o 
often  has  as  its  cause  a  psychic  trauma,  cither  a< 
nervousness,  theatrical  posing,  irritability  and  inn 
anee  of  remarkable  and  startling  symptoms  of  the 
life.  In  general  these  patients  show  lack  oi  BeH-e 
may  show  wonderful  will  power  or  obstinacy.  Si 
mata  of  hysteria;"  others  occur  only  rarely.  The  i 
catalepsy  (611),  globus  hystericus  (426),  emotioi 
oesophagus,  torticollis  and  other  spasms  (618),  h< 
(527), ovarian  tenderness,  photophobia,  tremor  (65 
itation,  anorexia  and  fasting,  tympanites,  phantO 
fever,  flushing,  sweating,  angio-neurotic  edema  (P. 
field  of  vision,  (866)  somnambulism  (1069),  doubl 

The  disease  occurs  as  the  result  of  traumatism  asso 
injury.  It  very  rarely  occurs  when  a  severe  physi 
cases  where  pecuniary  compensation  may  be  ODta 
cciving  any  compensation.  The  disease  is  closely 
scribed  above  under  hysteria.      Tremor,   fibrillary 

paralyses  (motor  and  sensory),  palpitation  and  va 

are  insomnia,  especially  in  the  early  morning  hou 
symptoms  can  be  simulated,  and  as  many  of  these 
scious and  unconscious  .simulation.  Simulation,  In 
in  "suggestion,"  as  in  hysteria. 

All  the  various  forms  ol    insanity  described  in  the  next  chart  exhibit,  and  are  in  part   dependent 


Ml 


lit  of  an  accident. 


SIS  OF  SYMPTOMS 


TV,  AND  WEAKENED  MENTALITY 

'  SYMPTOMS 

ire.    Eyelids  are  closed  and  resist  attempts  to  open  them.    Coma  can  usually 

Even  in  the  apparent  coma  the  patient   is  suggestible  and  close  obser- 

surroundings  and  therefore  not  truly  comatose.  Such  a  condition  may  result 
somnambulism,  trance 

an  allied  condition  from  auto-  or  foreign  suggestion,  or  from  wilful  deception. 
i  -mnl ar  states  quite  distinct  from  the  normal  life.  In  the  hypnotic  or  allied 
omatons.  This  is  a  very  rare  condition  and  offers  much  opportunity  for  deoep- 
;o  unconscious  suggestion  on  the  part  of  the  physician. 

implicated  acts  and  leads  a  life,  during  hours,  days  or  weeks,  of  which  he  later 
he  can  remember  v.  hat  happened  in  previous  similar  states  is,  to  say  the  least, 
n  automatic  acts. 

system,  especially  of  the  brain,  associated  with  an  increased  irritability, 

i  but  more  bo  in  women.    The  patients  are  either  incapable  of  exertion  or  tire 

i;  BO  that   they  arc  discouraged  before  they   undertake  it.      Their  memory  and 

ile.  apprehensive  and  have  a  Dumber  of  peculiar  fears:  phobias  (235 — agora- 
tic  of  neurasthenia  as  are  the  phobias,  arc  indecision  and  lack  of  will  power. 
h-motor  disturbances,  pares!  hesiae,  headache,  backache,  neuralgias  and  diges- 
ithenia  are  apprehension  and  fear    phobias). 

■  neurasthenia  and  i-  greatly  depressed  by  reason  of  an  abnormal  state  of  sclf- 
manently  lived  upon  the  condition  of  his  body  or  of  In-  mind       Patient   IS  de- 

diaease  or  abnormality  of  some  organ  of  his  body,  generally  the  viscera,  winch 
icdieal  examination  no  abnormality  can  be  discovered  adequate  to  justify  the 
patient's  mind.  These  false  judgments  are  very  various  and  are  often  mon- 
like  an  on  of  the  neurasthenic  phobias.    The  patients  are  anxious 

on  their  ills.     The  essentia]  symptom  of  hypochondriasis  is  a  fixed,  constant. 

is  diseased 

dren,  and  the  symptoms,  which  may  apparently  affect  any  part  of  the  nervous 
,e  imaginary  "|!  "'  :l  l:''~''  "'''''  (delusion    2]j5).  or  of  suggestions 

•ceived  from  others  or  from  some  abnormal  sensations  within  the  body.    The 

.cite  wonder  and  admiration  that  thej  are  not  very  scrupulous  in  their  mean- 
be  placed  on  then-  statements  The  reaction  of  tbi  patients  to  external 
irmal  m  its  results  The  symptoms  of  the  disease  are  bdtii  man]  and  variable 
itor  paralyses,  convulsions,  spasms,  contractures,  vaso-motox  and  secretory 
rmanent,  producing  a  confused  and  constantly  varying  picture  of  disease,  which 

or  chronic,  m    more  frequently  both.      In  addition   t..  the  i-hroni indition  of 

•d  suggestibility,  the  course  of  the  disease  is  interrupted  by  the  sudden  appear- 
atest  intensity,  w  hich  render  the  patient  helpless  and  often  apparently  threaten 
rol,  but  in  the  production  and  maintenance  of  some  prominent  symptom  the] 
of  these  symptoms  occur  ,-,o  frequently  that  the]  have  been  called  the  "stig- 

i  import  ant  of  these  acute  hysterical  attacks  ar vylsion  (586),  coma    1069 

ittacks  of  laughing  or  crying,  aphonia  748,  769)  mutism  717'.  stricture  of 
kneetbeeis  and  ii-  transference    I  653,  792),  paralysis 

spinal  irritation,  clavus  960),  cough,  dyspnoea  palpitation,  vomiting,  regurg- 
uuior.  false  pregnancy,  peritonitis,  anuria,  polyuria,  uielaniiria,  hemorrhages. 
,  blindness  851a  .  deafness,  (924),  anosmia,  ageusia,  concentric  limitation  ol 
msciouanese    1039     etc 

ed  with  great  fright,  or  m  -one-  accidents  from  fright  alone  without  ph 
injury  has  been  received.    It  is  especially  common  in  railroad  accidents  and  in 

1  for  the  injury;  although  it  ui  et  where  there  i-  no  hop. 

ied  to  neurasl  hernia  and  h;  I  be  sj  mpton 

m,  e-peci.ilK  nftei  exertion,  vertigo,  paresthesiae,  i"  local 
uotor  disturbanri  -  are  common  symptoms     Quite  characteristic  ol  the  di 
and  a  melanchohc,  hypochondriacal,  menial  state      Most,  if  no)  all.  of  the* 
ing  to  recovei   damages,  there  is  natural!]   more  or  less  of  con- 
far  from  expl inn  the  traumatic  neurosis. tin-  kev  to  which  ins  rathe 


i»i  \<;xosis 

Hysterical  Coma  (107  I 


Hysteria  (1074). 


Epilepsy  (1058;. 


Neurasthenia,  Psychasthenia    113,  L55,  161,  163,  178,     1072 
180,  671,  674,  843,  845,  959  970,  1033  , 


Hypochondriasis  (216). 


Hysteria  111.  128,  L30,  153,  179,  345,  125-6,  527,  586, 
618,  628,  664,  674,  747-8,  759,  793,  834,  843  B48, 
866,  878,  924,  926    960,  971,   hhki.   1033,   1069-70, 

107.-. 


Traumatic    Neuroses      Si timi  uimatic 

Hysteria    156,  816,  674,  I 


on,  a  weakness  ol  tin   mental  powers,  varying  in  degrc 


CHART  XVI  c 

Insanity 

Comprising  Numbers  Kill  on  left  side  of  Chart 
and  L076  to  111?  on  right  margin 


191 


DIAGNOSTIC  SYMPTOMS  AND  TESTS 


E 
X 
T 
R 
E 
M 
E 

D 
E 
F 
E 
C 
T 

I    -> 
N 

I 
X 
T 
E 
L 
L 
I 

G 
E 
N 
C 
E 


1076 

Amenlia  (211). 
More  or  less 
complete 


1077 

Dementia  (212) 
More  "i'  less 
^complete. 


107S 

Hallucinations  are 
abundant  and  domi- 
nant. Hallucinatory 
Insanity  (213). 


1079 
Delusions  are  present 
and  dominant.    Delu- 
sional Insanity  (215) 


1080 

An  exaggerated  emo- 
tional    state    ie    thi 
mptom. 
Emotional      I 

of    flu' 
have    been 


condition  in  which  the  mind  has  not 
developed  with  advancing  age,  due 
to  a  disease  of  the  brain,  either  congen- 
ital  or  acquired  in  infancy.    Besides  the 

mental  defect,  these  patients  often 
present  many  and  various  physical 
and  deformities  such  as:  de- 
formed skull,  posterior  hydrocephalus, 
high  palatine  arch,  coarse  body,  de- 
formed ears,  etc.  The  amentia  may  be 
either  general  or  partial,  and  some  of 
its  slighter  degrees  may  be  due  in  part 
to  defective  training. 


Occurring  in 
youth,  at 
puberty  or 
before  25  or 
30  years. 


A  condition  in  which 
the  mind  has  developed 
to  a  certain,  even  a 
high,  degree  of  intelli- 
gence and  then,  in 
consequence  of  disease 
of  the  brain  (functional 
or  organic),  all  mental 
development  has  not 
only  leased,  but  there 
has  been  a  distinct  re- 
nin, which  may 
go  on  to  a  complete 
loss  of  intelligence. 
Memory,  emotions  and 
interest  are  all  lost.  Pa- 
tient becomes  apathet- 
ic, reacts  to  no  stimula- 
tion, soils  himself  and 
does  not  even  eat. 


Usually    occur- 
ring in  adult  life 

alto-   l:."i  years, 

but    may    OCCUT 

in  youth. 


Occurring  in 
old  age. 


Patients  Bhow  little  or  no  intelligence.  Are  unable  to 
urine  and  feces.  About  their  only  desire  is  thai  J 
Most  of  these  patients  exhibit  frequent  and  violent 


Patients  can  talk  and  are  more  or  less  cleanly  in  their 
They  are  incapable  of  much  education.  They  can  f 
and  the  sexual  instinct  is  often  strongly  developed. 

Patients  show  a  degree  of  intelligence  approaching  tE 
children  develop  up  to  a  certain  point,  but  then  si 
ing  eyes,  thick  fissured  tongue,  and  short,  stubby  fins 
tobacco.      Simple  infantilism    is  often  called  "  atele 

Certain  feeble-minded  persons  seem  incapable  of  appi 

Complete  apathy,  coming  on  more  or  less  acutely.  O 
tion.  Appears  to  be  anesthetic  and  analgesic.  The 
cases  recover  after  several  months. 

Partial  apathy.  Patients  are  dull  and  stupid  but  consc 
is  an  absence  of  emotions  and  of  inte.jst  in  anythir 
They  perform  frequently  spontaneous,  impulsive,  sil! 
of  a  phrase  which  they  have  just  heard  or  spoken  (e 
The  varieties  under  this  head  merge  into  each  other 

'History  of  alcoholism  and  usually  associated  with  mult 

History  of  alcoholism  extending  over  many  years.  T: 
amounts  of  alcohol.    The  symptoms  at  times  resemb 

History  of  very  numerous  epileptic  seizures.     Gradua' 

History  of  a  previous  psychosis  which  has  gradually  pr 
(apathetic  dementia)  but  some  cases  show  great  rest 

History  of  syphilis.  Lumbar  puncture  shows  globuli 
inability  for  continuous  mental  concentration,  reel 
at  least  cheerfulness,  in  spite  of  the  illness  which  pail 
dementia.  No  paralysis,  but  much  paresis  and  esj 
tabes,  more  rarely  with  various  forms  of  spinal  scle: 

Associated  with  physical  weakness  and  with  atheroma 

loss  of  memory,  especially  for  recent  events,  with  ret' 

Blood  tension  often  high. 


A  condition  in  which  the  patient  is  constantly  receiving 
false  perceptions  from  his  different  senses:  either  visual, 
auditory,  olfactory,  gustatory,  tactile  or  painful,  or 
from  several  or  all  combined.  Associated  with  this  is 
always  a  certain  degree  of  impairment  of  conscious- 
ness, which  weakens  his  judgment  and  does  not 
permit  him  to  decide  that  these  hallucinations  are  false. 


A  condition  in  which  the  patient  has  formed  a  false 
judgment  about  things  which  concern  him.  The  basis 
of  these  false  judgments  is  partly  a  congenitally 
defective  brain  and  partly  hallucinations.  Associated 
with  these  delusions  there  is  always  present  a  vary- 
ing degree  of  impairment  of  intelligence,  which  pre- 
vents the  patient  from  recognizing  the  falseness  of  the  de- 
lusion when  evidence  is  presented  to  him  which  would  be 
adequate  for  a  normal  man;  although  many  of  these 
patients  in  their  own  way  reason  shrewdly.  These  delu- 
sions lead  to  irrational  conduct  on  the  pari  of  the  patient 
which  would  not  be  irrational  were  the  delusions  true. 


•Patient  is  overwhelmed  by  a  large  nun 
intentions  towards  him.     He  does  fo' 

History  of  alcoholism.      Patient's  halli 
Great  fright.      Violent  attempt  to  ei 

Many  other  poisons  besides   alcohol:  i 
produce  a  mild  hallucinatory  insanity 

Disease  commences  with  fever,  headacl 

•History  of  alcoholism.     Patient  has  for 
men  is  that  their  wives  are  unfaithfu 

Patient  has  delusions  upon  which  he  b 
is  not  built  upon  them.     Curable  in 


Patient  has  a  number  of  delusions,  u: 
systematized  or  nearly  so  but  whi( 
are  strong  enough  to  influence  his  coi 
duct  and  bearing.  Curable  in  most  case 

Patient  lias  many  delusions  which  arc  c 
and  are  woven  in  with  the  delusions  ill 
Bions  are  thus  systematized  and  some 
himself  as  a  mosl  remarkable  person 
delusion  of  persecution  (every  happ 


Exaggeration   of  the   sometimes   natural 
oi    discouragement 

with  life. 

Exaggi  ra  i    natural    feeling    of 


Patient  is  constantly  in  a  depressed  and  painful  frami 
by  the  patient  to  explain  the  melancholy:  the  co 
are  very  prone  to  suicide.     Their  circulation  and 

are  constantly  in  a  joyous  and  excited  mood  I 
and  due  to  delusions  (1111).    Mania  is  dh  idi  4  | 


son, 

i 


{Alternations  at  long  intervals  of  mania  ami  melanrhoB 
of  excitement  or  of  depre    ion  n icui 
Kraepelin  has  incorporated  all  of  th  rider  the  tei 


DIAGNOSTIC  ANALYSIS  OF  SYMPTOMS 


ABSTRACT  OF  SYMPTOMS 


ik  intelligibly,  but  are  often  noisy.  Many  are  unable  to  walk-.  Usuallysoil  themselves  with 
ood.  They  can  do  no  act  requiring  intelligence  and  are  incapable  of  sustained  attention, 
reaks  of  anger.     Many  of  them  are  undersized. 


I  Associated  with  hydrocephalus.     Fontanelles  and  sutures  are  unusually  open  and  broad.     Bra 

I      culous  sclerosis  with  nodules. 

|  Associated  with  epilepsy. 

■{  Associated  with  a  very  small  skull.     Brain  usually  weighs  loss  than  1000  grammes,  or  33  ounces. 

j  Occurring  in  family  groups,  with  blindness  and  optic  atrophy  and  dark  red  spot  in  place  of  macula  lutea. 

Associated  with  congenital  hemiplegia  or  diplegia  and  with  rigidity  and  convulsions  (501). 
{  Associated  with  no  special  characteristic. 


f  All  the  classes  above  given  under  idiocy  but  with  less  extreme  mental  defect. 


■t„     Thev  exhibit  in  their  acts  an  evident  though  low  degree  of  intelligence.  J  Very  defective  intelligence  in  general,  but  in  certain  directions  (usually  music  or  mathematics)  may  show  great  skill, 
few  abstract  conceptions  and  no  high  moral  ideas.     Masturbation  is  common  1  Associated  with  destruction  or  atrophy  of  the  thyroid  gland.    Arrest  of  growth.    Thick,  dry  and  scaly  skin.    Coarse  features  (1164). 

(  Associated  with  no  special  characteristics. 

■mal  but  are  evidently  below  the  standard.  They  cannot  be  educated  beyond  a  certain  point.  They  are  often  obstinate  and  of  violent  temper  upon  provocation,  even  though  in  general  amiable.  Some 
nd  never  advance  further  (infantilismus).  In  some  cases  of  infantilismus,  there  is  a  defective  growth  of  the  body  with  a  email  head  and  a  peculiar  characteristic  Tartar-like  expression  of  the  countenance,  slant- 
They  possess  great  faculty  of  imitation  (Kalmuck  idiots  or  mongolismus).  This  disease  presents  many  resemblances  to  cretinism  (1090,  1164).  Infantilism  may  be  due  in  some  eases  to  poison,  such  as  wine  or 
"      Infantilism  with  premature  senility  is  called  "  progeria." 

iding  the  simplest  moral  ideas,  although  their  mental  defect  is  not  so  obvious  in  other  directions.     On  closer  examination,  however,  a  general  mental  defect  becomes  evident. 

ousness  is  obscure.  Patient  incapable  of  any  mental  effort.  Is  in  a  dream-like  state,  immobile  and  does  not  appreciate  what  is  going  on  about  him.  Will  answer  no  questions  and  will  respond  to  no  stimula- 
e  no  hallucinations  or  delusions.    The  cutaneous  reflexes  are  lost  and  the  tendon  reflexes  are  exaggerated.    The  course  of  the  disease  is  interrupted  at  times  by  periods  of  excitement.     More  than   half   of   such 


shows  a  tuber-        Hydrocephalic  Idiocy. 

Epileptic  Idiocy. 
Microcephalic  Idiocy. 
Amaurotic  Idiocy. 
Porencephalic  Idiocy. 
Idiopathic  Idiocy. 

Imbecility 
Idiot  Savants. 
14).        Cretinism. 

Idiopathic  Imbecility. 


1081 
Idiocy 
(743) 


10SS 
Imbecility. 


Moral  Imbecility  or  Habitual  Criminals. 
Primary  Dementia  and  Stupor. 


1092 
The 

Feeble- 
Minded 


1083 
1084 
10S5 
1086 
1087 

1088 
1089 
1090 
1091 


1094 
1095 


ness  is  fairly  clear  and  they  appreciate  what  is  going  on  about  them.    Hallucinations  and  delusions  are  common.     There  rSimple  progressive  mental  deterioration,  at  times  permanent,   often   temporary,    com- 

inesthesia  and  analgesia.    They  are  unwilling  to  perform  any  act  and  offer  resistance  when  forced  to  do  it  (negativism).  mencing  at  puberty. 

its.    They  often  repeat  the  same  act  or  the  same  words  many  times  (stereotypy).     They  also  often  repeat  the  last  word  ■<  Alternating  conditions  of   stupor   and   excitement,    negativism,    stereotypy,   echolalia 

lia),  or  repeat  obscene  words  (coprolalia),  or  repeat  an  act  (echopraxia),  or  remain  in   any   given   posture    (catalepsy).  with    steady  mental  deterioration,  at  times  permanent,  often  temporary, 

all'show,  as  prominent  symptoms,  impulsive  ideas  and  acts.     The  prognosis  is  uncertain.  [Hallucinations  and  partially  systematized  delusions  with  steady  mental   deterioration. 

leuritis,  except  in  very  rare  cases.    A  peculiar  loss  of  memory  with  a  bringing  of  memories  of  the  remote  past  up  to  the  immediate  past  (retroactive  amnesia — 769),  failure  to  appreciate  the  relations  of  time  and  space. 

'.  Dysarthria.  Loss  of  memory  and  power  of  attention  and  mental  power.  Delusions  are  frequent.  Normal  and  ethical  ideas  blunted.  Irritable,  sentimental  and  often  very  susceptible  to  the  effects  of  small 
Dse  of  paresis  (1104)  (pseudo-paresis),  but  the  dementia  is  less  pronounced,  the  cerebro-spinal  fluid  is  normal  and  improvement  follows  abstinence  from  alcohol. 

of  memory  and  mental  power.     Masturbation  is  common.     Usually  steadily  progressive  and  incurable,  but  this  dementia  may  occur  in  childhood  and  may  be  transitory,  in  which  case  it  may  be  cured  by  bromide. 

into  a  condition  of  apathy  and  more  or  less  complete  loss  of  intelligence.  Patients  may  carry  over  into  this  stage  some  traces  of  the  emotions  and  delusions  of  the  former  psychosis.  They  usually  sit  motionless 
ess  (agitated  dementia). 

I  lymphocytosis  in  cerebro-spinal  fluid.  Wassermann  usually  positive..  Argyll-Robertson's  phenomenon  and  often  unequal  pupils.  Tremor  of  lips,  tongue  and  hands.  Loss  of  memory,  loss  of  self-restraint, 
less  and  change  in  character  are  early  symptoms.  Speech  blurred,  slovenly  and  tremulous.  Words,  syllables  and  letters  left  out  in  speaking  and  in  writing.  Restless,  excited  and  irritable,  with  exaltation  or 
rarely  recognizes  as  existent.  Grandiose  delusions,  silliness  and  inconsistency  in  striking  contrast  with  inordinate  pretensions.  Gradually  increasing  physical  and  especially  mental  weakness  up  to  complete 
y  apraxia  (230,  2S2).     Careless,  inconsiderate,  slovenly  clothes,  etc.     Apoplectiform  and  epileptiform  seizures  are  usually  present  in  the  course  of  disease.    Incurable,  but  remissions.    Frequently  associated  with 


Hebephrenic  form. 
Catatonic  form. 

Paranoid  form. 
Korsakow's  Psyche 
Alcoholic  Dementi; 


1096  1097 

Adolescent  Insanity  or  the 
so-called  Dementia  Precox        1098 
(a  term  of  very  doubtful 

value).  1099 

1100 

1101 


(65S,  1107,  1109) 


Epileptic  Dementia,  (575,  1058). 
Terminal  or  Secondary  Dementia. 


Paresis.  General  Paresis.  Paralytic  Deineniia, 
(134,  177,  416,  419-20,  579,  675,  763,  895,  1049, 
1216,  1230). 


1102 
1103 


arteries.    The  dementia  varies  from  day  to  day  greatly  in  degree  and  may  lead  the  patient  to  do  very  foolish  things  (often  erotic),  while  apparently  sane.     Loss  of  will  power  (drunkenness).     Depression  and 
n  of  past  memories.     Dread  of  impending  poverty.     Desire  to  go  home,  imagining  himself  to  be  in  a  strange  place.      Restless  at  night,  associated  with  hallucinations  and  delusions.      Attacks  of  excitement. 


Senile  Dementia. 


1105 


nd   especially  doubts   their 


of  hallucinations  which  cannot  be  reconciled  with  his  previous  experiences.      He  becomes  confused,  frightened  and  timid.      Doubts  his  own  identity  and  that  of    those   about    hii 
acts  which  might  be  rational  were    his  hallucinations  true.     May  be  the  early  stage  of  other  forms  of  insanity.     Probably  a  form  of  moderate  delirium. 

ions  are  of  all  kinds  but  are  usually  visual  and  concern  snakes,  spiders  and  other  small  grotesque  and  repulsive  animals.     Tactile  hallucinations,  shown  by  fumbling  of  the  fingers,  also  are  usually  very  evident. 
:  from  his  enemies.      Pronounced,  continuous  tremor  and  insomnia.     Disease   usually  lasts    less  than  a  week  and  usually  terminates  in  recovery. 


•  exogenetic,  such  as  belladonna,  salicylic  acid,  etc.;  or  autogenetic,  such  as  uremia,  cholestrin,  pti 
lelirium,  wrhich  may  last  a  few  hours  or  days  or  may  continue  during  weeks,  months  or  years. 


•  septic  (post-febrile  insanity),  especially  when  the  poison  acts  upon  an  exhausted  i 


Confusional  Insanity. 

Delirium  Tremens  (1101,  1109). 

Toxic,  Septic  or  Post-febrile  Insanity. 


lazed  feeling   and  delirium,  followed  by  violent  excitement  and  violent  actions.     Many  hallucinations.     Speech  is  continuous,  violent  and  incoherent.     Disease  usually  terminates  fatally  u 

,  on  the  basis  of  hallucinations,  more  or  less  permanent  delusions,  especially  of  jealousy  and  persecution.      These  are  often  so  exaggerated    and   monstrous    as   to    be   grotesque.     A  very   common  delusion 
atients   often  act  violently.     Some  alcoholic  tremor.     Curable,  and  usually  lasts  less  than  a    month  after  alcohol  has  been  withheld. 


•  three  weeks.        Acute  Delirium  or  Delirium  Grave 


Acute  Alcoholic  Mania.    Alcoholic  Hallucinosis 
(1101,  1107). 


These  delusions  are  not  associated  with  any  decided  emotional  manifestations  and  are  at  times  permanent,  at  times  changeable;  but  they  are  not  reasoned  upon  shrewdly  and  a  systematic  theory       Simple  Delusional  Insanity. 


These  delusions  are  of  a  pleasant  exhilarating  nature  impelling  to  action,  to  talk  and  incidentlyto  the  disregard  of  the  right  of  others.     These  patients  are  usually  violent  and  dangerous  to  themselves  and  others. 

These  delusions  are  of  a  depressive  nature  and  tend  to  inhibition  of  action  and  speech,  to  self-abasement  and  to  self-destruction.     The  patients  sometimes  seem  to  be  in  actual  stupor  (melancholia  cum  stupore) 
or  merely  profoundly  depressed  with  inhibition  of  all  action  (melancholia  attonita).    At  times  the  intensity  of  their  grief  drives  them  to  frenzy  and  breaks  through  their  inhibition  and  impels  them  to  deeds 
k.    ot  violence  (raptus  melanchohcus).    Occasionally  there  is  restlessness  (melancholia  agitata).     All  these  conditions  seem  to  be  the  direct  result  of  delusions.     Such    patients  are  very  prone  to  suicide. 

the  result  of  hallucinations.  They  are  fixed,  permanent  and  are  reasoned  upon.  Newspaper  paragraphs  on  indifferent  subjects  and  various  circumstances  in  the  entire  life  of  the  patient  are  more  or  less  distorted 
ji tempi  el  an  explanation  ,,t  i lie  curious  things  ulueli  are  happening  to  the  patient.  The  patients  reason  very  clearly  and  if  their  premises  are  granted  it  is  almost  impossible  to  answer  their  arguments.  The  delu- 
i  nieoij  is  e\t.iv,.,|  lo  explain  lliein.  1  lie  most  trivial  happenings,  even  in  the  remote  past, are  fitted  into  this  system  in  the  most  surprising  and  ludicrous  way.  The  general  result  is  that  the  patient  regards 
Jiise  so  niai,\  persons  busy  themselves  about  his  affairs.  In  typical  cases  the  patient  evolves  first  a  delusion  of  observation  (all  things,  even  the  most  indifferent  and  remote  have  reference  to  him);  next,  a 
to  injure  nun  or  to  try  his  character),  and  finally  a  delusion  of  grandeur  (he  must  have  a  great  destiny  when  so  many  persons  seek  to  injure  him  or  to  tempt  him). 

ind  for  which  there  is  no  discoverable  adequate  cause— "a  cloud  settles  over  the  mind."  A  pessimist.  No  hallucinations,  no  delusions,  except  such  as  are  secondary  to  the  depressed  frame  of  mind  and  invented 
ifrlilv  ■  '  ".'l,a""'";i1,11'  sm,  etc.  there  is  an  inhibition  of  mental  and  physical  activity.  Patients  withdraw  themselves  as  much  as  possible  from  the  world.  They  sit  quiet  and  are  pictures  of  woe.  They 
'Ociuy  functions  are  greatly  disordered.     Curable.     The  secondary  form  of  melancholia,  due  to  delusions,  has    been  described  under  1112. 


Symptomatic  or  Delusional  Mania. 
Symptomatic  or  Delusional  Melancholii 


Primary  Melancholia. 


iut  any  discoverable  adequate  cause.    Optimistic.   They  have 
a  mild  form  (maniacal  excitation)  and  a  severe  form  (frenzy) 

h  usually,  but  not  alwayi 


Mania  is  often  sympto-       Primary  Mania 


comparatively  normal  period  between  the  two.    The  duration  and  the  intensity  of  the  attacks  and  the  duration  of  the  interval  i 


WnSi  L™iy-!lltm,at';  ••,,er A ,'onger  or  sl,orte,r  interval  (circular  insanity).     In  some  cases  the  excited  and  depressed  phases  are  commingled, 
maniacal  depressive  insanity    but  the  permanence  of  this  term  is  doubtful.    His  classification  involves  a  recasting  of  the  nomenclature  of  mental  dis, 


■  the  alternations  are   momentary,  giving  a 
ses,  and  it  is  doubtful  if  the  time  is  yet  ripe  for  s 


lixed   form." 
lan  attempt. 


Circular  Insanity. 

Maniacal  Depressive  Insanity 


1106 

1107 

1107a 

1108 
1109 


1111 
1112 


1116 
1117 


CHART  XVII 

Trophic  and  Sympathetic  Disorders 


DIAGNOSTIC  ANALYSIS  OF  SYMPTOMS 
TROPHIC  DISORDERS  AND  DISORDERS  OF  THE  SYMPATHETIC  SYSTEM 


Symptoms  Analysed 


1120 

Trophic  Lesions. 


1121 

Disorders  of  the  Sympathetic 

System. 


Tissues  Involved 
fll22 
Muscular  Tissue. 

1123 

Cutaneous  and  Sub-Cutaneous  Tissue. 


1124 

Fattv  Tissue. 


1125 

Bone  Tissue. 

1126 

Joint  Disease. 

1127 
.Other  Trophic  Lesions. 

rll28 
Ganglionic  Disorders. 

1 1129 

(.Vaso-Motor  Disorders. 


See  Chart  XVII  a. 
See  Chart  XVII  b. 

■See  Chart  XVII  c. 


VSee  Chart  XVII  d. 


193 


CHART  XVII  a 

Muscular  Atrophy  and   Hypertrophy 

( lomprising  Numbers  1 122,  1 130  and  l  131  on  left  aide  of  <  hart 
.■mil  1 1  It;  to  l  L56  on  righl  margin 


DIAGNOSTIC  ANAL  I 


HI  \<;.\<>STIC  S\  M1TDMS    \\H    1  I  <l  s 


MUSCULAR  ATROPir 
ABSTRACT  I 


i  L30 
Vlliol'llY 


II.' J 

Ml  BC1  LAB 

i  tssi  i 


L131 

in  II  i:  i  inH'in 


tively 
onset 


rapid    in 


Muscular  atrophy. 

Lesion    of   peri- 
pheral motor- 
neurone 


Atrophj  is  great  in 
degree    and     rela- 


Atrophy  is  slight 
in  degree  and  very 
slow  ui  onset. 


Muscular    atrophy 
:mil    hypertrophy 
combined. 

Lesion  in  muscles. 

Lesion    in    central 
motor-neurons. 


'Increased  strength.      No  lesion 


Istrength 


Lesion   in   muscle 


Acute   and    suli- 
acute    course, 
(inflammatory 

lesions). 


Chronic  course, 

(degenerative 

lesions). 


Paralysis  is 
mary  aymp 
atrophy  is 
dary  to  it. 


Atrophj  is  i 
in:ir\  sympti 
the  paralj  i 
seconder]  ti 
consequent 

upon  It . 


Associated  with  chronic  join 

neuritis  cm  be  found. 

Muscles  <>r  face  (Landouzy-Dejerin 
form)  are  first  affected  Some  a 
atrophied,  a  few  hypertrophied, 


Paralysis  Is 

and 

is  secon 


Very  slow  course. 


Muscular   fibers 
normal,       A    true 
hypertrophy. 


The  hypertn 
Tin-  hypertn 


(  'alf    muscles,   infr:i-s|)ili:i1 

trophy.    ( Hlicr  muscles  are  botl 
generation:  some   atrophied, 
atrophied.     Legs  are  early  and    i 


IS  OF  SYMPTOMS 


ND  HYPERTROPHY 
SYMPTOMS 


m       <  omplete    01    par- 
ri' i      tial  electrical 
hi-      reaction  of 

degeneration 


nc!        linn; 

electrical  excitabil- 

i >■  1         it]  .  hill   DC 

"i  degeneration: 


History  of  injury,  wound,  bruise  or  scar. 

Limited  to  distribution  of  one  nerve  (simple  neu- 
ritis) or  many  nerves,  (multiple  neuritis).  Usu- 
ally associated  with  m'Iisoia    -\  inptoins:  pain  and 

anesthesia,  nerve  and  muscle  tenderness. 

(I roups    of    muscles    attacked    not    corresponding    to 

the  distribution  of  any  nerve.  No  sensory 
symptoms,  except  some  pain  at  onset  in  back, 
joints  and  muscles.  Very  rarely  nerve  and 
muscle  tenderness.    Globulin  and  lymphocytosis 

in  cerebrospinal  fluid  in  acute 

\tlophv  affects  either  the  alius  or  the  leji>.  Selixin 
and  other  symptoms  of  myelitis  ale  present. 
Organic    reflexes    are    more    or    less    disordered. 

Superficial  and  deep  reflexes  are  abolished  in  the 
paralyzed  area. 

Vtrophy  Commences  in  the  small  muscles  of  hands. 

Or  muscles  of  shoulder  girdle,  and  extends  and  is 

■led    with    fibrillary    contractions.      Mild 
spastic  paraplegia    525,  797)  in  leys 

Atrophy  affects  the  muscles  of  tongue  and  lips  and 
ociated  with  fibrillar]   contractions,     Mild 
spastic  paraplegia  (525,  79?)  in  leys 

Airophj  affects  the  hands  usually.  Is  associated 
with   dissociation   of   sensation   and   often   with 

on     uid   mutilation. 


DIAGNOSIS 
Injury  of  nerve  (489,  822). 


1  I  16 


Neuritis    (488-92,    822,    1)40-8 ).     1147 
(Figs.  33,  38.) 


Vcute   anterior  poliomyelitis  1  1  t^ 

(495,789).     (Figs.  28-7.) 


Myelitis  of  Cervical  or  Lumbar  1 1 18s 
Enlargement  (48.5,  549) 


Amyotrophic    lateral    sclerosis     1149 
(547  695,  797)     (Figs.  26-7.) 


<  limine  bulbar  paralysis  (646,     1 150 
'I'M         Figs  21-2.) 


Syringomyelia  (552,693,  837-9,  1150a 

1009,  1170,  1357-9). 


especially  with  ankylosis,    Many  of  these  cases  are  neuritic,  but  in  > s  no      Arthritic  atrophy. 


of  shoulder  girdle  i  Krli.-  juvenile  type  .  or  of  legs  (pseudo-hypertrophic 
es  apparently  hvperi rophicd  Excised  muscle  fibers  show  degeneration:  some 
increase  of  interstitial  fat      No  fibrillary  contractions. 


,h3 


The  atrophj 

entirely     to    ■■ 

No  electrical  reac- 
tion of  degenera- 
tion. 


The  reflexes  are  exaggerated      Ankle-cl i      ind 

are    present    when    legs    are  affected, 
unless  prevented  b]  conl  rat  I  uret 


Muscular  dystrophies  (477  786,     1152 
1156) 


A    paralysis   of   long  standing,     1163 
especial!]  one  from  infano] 


result  of  much  exercise, 
is  due  to  irring  at  the  commencement  ol  voluntary  motion 


Strong  man  or  al hlets  1 1"1 1 

Thomsen's  diss  ise  (613  1 166 


id   -nine  other  mils'  ll  rge,  but  are  w<  ■  1 1  •  n  i    hyper- 

Ik  and  atrophied      No  fibrillar]  contraction      Excised  muscle  Boers  show  de- 


vpei trophied  and  much  interstitial  fat 
l\  affected. 


out  •       \ll  muscles  are  finallj 


Pseudo-hj  pertrophic 

500     and    the    iiiii-  ul  ii    d\  - 

trophies  (118 


CHART  XVII  b 

Cutaneous  and  Sub-cutaneous  Trophic  Disorders 

Comprising  Numbers  1 123  and  1  132  to  1 L3S  on  left  Bide  of  Cnarl 

and  11(30  to  1173  on  right  margin 


197 


DIAGNOSTIC  ANAL  il 


CUTANEOUS  AND  SUB-CUTANEt 


DIAGNOSTIC  SYMPTOMS  AND  TESTS 


112.3 

CUTANEOUS 
AND  SUB- 
CUTANEOUS 
TISSUE 


1132 

Atrophy. 


L133 
Hypertrophy. 


1134 
Eruptions. 


1135 


ABSTRACT  ( 
[The  skin  is  unusually  smooth  and  thin.  The  fingers  become  pointed. 

change  occurs  quite  frequently  in  nervous  diseases,  especially  in  t.l 

.  The  hair  falls  out,  either  all  over  head,  face  and  body  (as  in  syphilis) 
I  skin  is  not  changed  in  appearance.  Allied  to  this  condition  is  thi 
I     consequence  of  severe  pain,  or  psychic  shock,  or  unknown  cause 

JAtrophy  of  the  normal  pigment  of  the  skin;  so  that  patches  of  clear 

j  persons  of  dark  complexion.  The  edge  of  the  patch  is  more  deep] 
'-See  also  facial  hemi-atrophy,   1179. 

The  skin  and  mucous  membranes  everywhere  appear  thickened,  as  if  ii 
slightly,  on  pressure.  The  skin  is  sallow,  dry  and  scaly.  Patient 
body  and  features  are  enlarged.  Nails,  teeth  and  hair  break  ai 
heavy.     Voice  is  slow  and  hoarse.     Response  is  slow  and  intellect 

disordered.      The    thyroid    gland    is    atrophied     or    destroyed    by    I 

re val  of  t lie  thyroid  gland.     Arterio-sclerosis  and  interstitial  in 

Common  in  women  than  in  men,  and  frequently  occurs  at  the  time 
in  children  they  become  dwarfs.  The  cause  of  the  disease  is  th 
thyroid  gland  and  it  can  be  cured  by  the  administration  of  the  thy 

The  skin  is  thickened,  generally  or  locally,  infiltrated,  very  firm  an 
especiallj  at  their  ends,  and  the  fingers  become  much  shortened  ! 
in  women  than  in  men  and  seems  to  be  allied  to  myxedema.  Tin  dis 
ocdematosum)  and  ends  with  an  atrophy  of  the  indurated  patch  (, 

Clusters  of  vesicles  filled  with  clear  fluid,  each  cluster  upon  a  patch  i 
or  two  nerve  roots  and  strictly  limited  to  their  distribution.  Th' 
It  is  usually  accompanied,  preceded  and  followed  by  severe  pain  in 
pain  may  continue  for  months  after  the  rash  has  disappeared. 

In  some  forms  of  nervous  disease  (especially  in  hysteria)  elevated  pa 
always  when  the  skin  is  irritated  (urticaria  scripts  dermographia 
sometimes  do  not. 

Successive  crops  of  bullae,  which  are  at  first  small  vesicles  and  inereu- 
Several  vesicles  may  coalesce.      There  may  or  may  not  be  fever 
may  be  intense.      A  very  fatal  disease. 

No  spa 
the  a 


With  much   loss  of 
tissue. 


'Ulcerations  larger  and  smaller  with 
sloughing  and  loss  of  phalanges  and 
even  whole  lingers  and  toes.  The 
whole  process  is  painless  and  may 

in  part  be  the  result  of  traumatism 
in  the  analgesic  parts. 


scum! 
IHTVi 

Spastic 
turb: 
tore 
over 
syni] 


With    small    loss   of 

tissue. 

See  also  Raynaud's, 

diseasi     1 L95). 


Large,  deep,  sloughing  ulcers  commencing  wi 
patients  usually  suffering  from  motor  and  .- 
subjected  to  much  pressure  (sacrum,  trocha 
pulously  clean. 

\n  uli  .ration  usually  commencing  on  the  bal 
and  painlessly  extending  deeper,  until  in  u 
on  its  dorsum.  Such  an  ulcer  very  rarely 
which  ulcerates  and  the  pus  escaping  forn 
lary  reflexes  and  other  symptoms  of  tabes  ai 
in  the  urine  in  a  small  minority. 

Ulcerations  more  or  less  severe,  the  result  ( 
Bkin  is  often  bronzed.     Symptoms  of  neurit 


.  IS  OF  SYMPTOMS 


5  TROPHIC  DISORDERS 
I  SYMPTOMS 

k  curved  and  are  striated.    This 
in  which  the  peripheral  neurons  are  degenerated. 

<>nly  in  patches,  usually  on  the  head  and  face.  The 
rnmsi  white  of  the  hair  in  patches,  or  universally,  in 
i  of  haii  dye 

itc  appear.  They  are,  of  course,  most  noticeable  in 
igmented  than  the  surrounding  skin. 


DIAGNOSIS 


Glossy  skin. 

Alopecia,  (general  <>r  areata). 

Vitiligo  and  I.eucoderaaa. 


1160 
1161 

UG2 


rated,  and  do  nol  pit,  or  pit  but 

e  very  sensitive  to  cold.    The 
all  out.    The  movements  are 

ty  very  sluggish  and  at    times 

i-e.    The  disease  may  follow 

it  is  may  lie  present.      Is  more 

ie  climacteric.    When  it  occurs 

isence   of    the    seeretioli    of    the 

!  gland. 


<  lecturing 

adults. 


( Iccurring  in 

children. 


ird.    Tic  bones  of  the  phalanges  bee  ime  absorbed, 
abnormally  movable.    The  disease  is  more  common 

often  i urn-ices  :is  :i  loc:d  patch  of  edema  stadium 

limn  atrophicum).     At  times  patches  are  pigmented. 

I  lene  I  skin;  tin-  clusters  following  the  course  of  one 

uption  dm-,  up  ami  disappears  after  a  week  or  two. 

nerve,  along  the  com 1  which  it  is  situated.      The 


Myxedema. 

Cretinism  and  Dwarfs  (1090,  1177). 

Scleroderma  ami  Sclerodactyly. 

Herpes  Zoster.     Herpetic  Neuritis 


1163 


1164 
1165 


t,  white  or  red,  appear,  at  time-  spontane  tusly,  and 
Such  patches  of  urticaria  sometimes  itch  and 


Urticaria  (1201). 


1167 


an\  Bise.  appear  on  the  skin  and  mucous  membranes. 
burning  sensation-  and  the  pain 

symptoms  in  legs.     The  disturbances  are  limited  to 
tribution  ol  one  or  more  nerves.    All  forms  of 

V  are  abolished.      Small  tumors  may  occur  along  the 

inks,  together  with  other  manifestations  of    leprosy. 

nptoins    m    legs,    when,    a-    is    usual    the    tropin.  •   di  -- 
s  are  hunted  to  hand-  and  arms       I'am  ami  teinpeia- 

il   tactile  Bensibilit] ,  usuallj 
rea      Kj  phosit    ind  spondylitis  are  common 


Pemphigus. 


Leprous  Neuritis 


Syringomyelia    or    Morvan's   disease    (562,    693, 
lis:       (Figs.  26-7.) 


1168 

llti'.i 


1170 


nd  occurring  only  in  bed-ridden 
iry  paralysis,  and    occurring  almost  al  - 

,U:  n hi  a  the  parts  are  not  kepi 


Bed  Sores.     |  decubitus, 


the  foot,  not  growing  larger  superficially,  but  slowlj 
il  cxtoml    ■pi!'-'  through  the  fool 
illy  commenci 
-  jerk.   urgyll-Robertson's  pupil- 
rencnl  in  the  majoril  hile  sugar  is  pi 


Perforating  Ulcer  of  Tabes  and  (rarely)  Syringo 
myelia  and  I  linbi  j 


ighl   traumal  ism      In I    iraeni  al  neuritis,  the 

■  it . 


Neuriti  I  8,  II  I7i 


CHART  XVII  c 
Trophic  Disorders  of  Fat,  Bone  and  Joints 

Comprising  Numbers  1124  to  1127  on  lefl  side  of  Chart 

and  117")  to  NSs  on  ri<;ht  margin 


199 


DIAGNOSTIC  ANAL^ 


TROPHIC  DISORDER! 


DIAGNOSTIC  SYMPTOMS  AND  TESTS 


ABSTRACT  < 


1124 
FATTY 


TISSUE. 


1136 
Atrophy. 


|  1137 
^Hypertrophy. 


'Failure  in 
development. 


1125 

BONK  TISSUE. 


1138 
Atrophy. 


1139 
Hypertrophy. 


1140 
Fragility. 


One  of  the  earliest  symptoms  of  diabetes  mellitus  is  an  inability  of  the  l 

excess  of  fat  had  been  deposited.  Patients  lose  weight  and  if  the  dise 
urine  shows  the  constant  presence  of  sugar.    Atrophy  of  Fat  and  emaa 

Large  and  tender  deposits  of  fat,  in  lumps  or  in  layers,  widely  diffused  c 
Arms  and  legs  painful  and  tender,  especially  in  the  acute  stage  when  tl 
frequently  in  middle  aged  women  (often  alcoholic  or  syphilitic). 

Many  eases  OCCUT,  either  eongenitally  or  acquired  in  early  life,  in  which 
so  that   the  individuals  remain  throughout  life  of  abnormally  small  si  a 

due  to  atrophy  or  loss  of  function  of  the  thyroid,  or  pituitary,  gland. 

mally  formed  (simple  dwarfs  or  decidedly  undersized  men),  while  ot tl 
described  elsewhere,  under  infantilism  and  mongolism  (1093),  erelinisi 
(chondro-dystrophia  foetalis)  there  is  a  dystrophy  of  the  epiphyseal  <■ 
normally  in  length;  SO  that  dwarfism  results.      The  head  is  relatively  li 

especially  their  proximal  segment,  the  hand  is  short,  the  fingers  broad, 

lordosis,  pelvis  contracted,  legs  often  bowed  or  knock-kneed  and  joi 
developed.     Adults,  as  well  as  children,  not  infrequently  become  shorti 

in  the  legs,  as  in  rickets,  osteitis  deformans  (1182),  osteomalacia  (11!- 
kyphosis,   etc. 

In  cases  of  extensive  acute  anterior  poliomyelitis  and  of  cerebral  palsy  of  cl 
or  very  slow  growth  of  the  part  from  disuse. 

One  side  of  the  face  is  much  smaller  than  the  other,  due  to  atrophy  of  al 
fat.  The  process  is  usually  progressive.  It  seems  to  be  caused  by  inji 
neuritis.  Dryness,  scaliness  and  loss  of  color  of  the  skin  are  common 
small  area  atrophies,  which  atrophy  gradually  extends  laterally  over  il 
process  continues  until  the  entire  half  of  the  face  is  atrophied  and,  in 
parts  of  the  body.  One  side  of  the  tongue  is  usually  atrophied.  I'a 
the  atrophy. 

One  side  of  the  face  is  much  larger  than  the  other,  due  to  enlargement  of 
progressive,  and  seems  in  some  cases  to  be  due  to  a  periostitis. 

The  bones  of  the  head  and  face  arc  enlarged,  diffusely  or  nodulated,  and 
them.  Headache,  neuralgia,  blindness,  deafness  and  facial  paralysis 
are  not   enlarged.      Forehead  is  bulging  and  head  is  often  of  great  size 

Disease  commences  late  in  life  with  slight  pains,  especially  in  legs.  Th 
jaw  is  not  enlarged.  The  head  enlarges,  the  legs  and  vertebral  coliiii 
patients  become  shorter  (even  as  much  as  a  foot  or  more)  and  their  w: 

Symmetrical  enlargement  of  all  the  tissues,  but  especially  the  bones  of  tin 
etc.  It,  comes  on  gradually,  patient  requiring  larger  and  larger  gloves 
Shouldered"  (kyphosis).  These  changes  arc  often  associated  with  bib 
head  and  joints  is  a  common  symptom.  The  disease  is  caused  l.\  lr 
in  early  life,  before  the  epiphyses  arc  joined  by  bone  to  shaft,  gigantis 

The  hands  and  feet  are  enlarged,  and  the  lingers  and  toes  "clubbed."      Th 

by  the  X-ray.     These  symptoms  arc  associated  with  chronic  puhnonan 

*      toms  vary  greatly  in  degree  and  extent;  the  mildest  form  being  "clubl 

In  some  persons  the  bones  are  unusually  brittle  and  break  upon  the  sligh 
of  these  cases  occur  in  old  age  (senility),  others  occur  in  middle  life,  du 
malacia),  while  others  occur  in  children.  The  disease  causing  it 
thvrosis,  etc. 


1120 

JOINT  DISEASE. 


1127 

OTHER  TRO- 
PHIC LESIONS. 


Joints     painless,     enlarged,     abnormally     movable, 

especially  liy perextc nsinii,  cartilages  eroded,  effu- 
sion of  synovial  Quid,  exostoses  of  bone.  The 
exciting  cause  for  these  changes  is  often  painless 
traumatism,  at   least   in  part. 


(■Joint    involvement     not     un-  Knee-jcrl- 

common.    Usually  in  legs.  Bladde 

!  Joint  involvement  rare.   Usu-  Knee-jcrl 

tally  in  arms.  Loss  ol 


1141 

Atrophy  and 
hypertrophy. 


Atrophy  OT  hypertrophy  of  different  organs  (mammary  glands,  tongue,  etl 

quently  met  with  and  may  be  due  to  disordered  nervous  action,  but  tin 


S  OF  SYMPTOMS 


F  FAT  AND  BONE 

SYMPTOMS 

t •  >  deposit  fat  in  the  tissue,  although  previously  often  bo 
is  long  continued  Inn. mi-  emaciated.     Examination  of  the 

mi  occur  in  fevers  and  in  many  other  conditions. 

arms  and  legs.     Face,  feet  and  hands  not  much  involved. 
it  i-  being  deposited.     Locomotion  impeded.    Occurs  most 


DIAGNOSIS 
Diabetes  Mellitus  (900,  1172). 


1175 


Adiposis  Dolorosa.    Dercum's  Disease  (1012).  1170 


■  bony  framework  of  the  body  does  not  develop  normally; 
-  reason  to  believe  that  some  of  these  cases  are 

individuals  are  merely  small  but  otherwise  nor- 

show  many  physical  deformities.  Some  eases  have  been 
kMO,  1164)  and  microcephaly  [1084).  In  Achondroplasia 
■gas,  in  consequence  of  which  the  bones  do  not  increase 
the  bridge  of  the  nose  depressed,  the  arms  and  legs  short. 
■most  equal  length  and  divergent  undent  shape),  lumbar 

aluiormally  lax.     The  muscles  are  rather   unusually   well 

i  consequence  of  excessive  bowing  of  weakened  long  hones 

etc.    and  in  consequence  of  curvature  of  the  spine,  08   in 

hood  occurring  in  infancy  there  is  often  an  arrest  of  growth 

even  of  the  hones,  and  especially  of  the  skin  and 

or  cold  and  in  some  cases  is  due  to  a  trigeminal 

(Btoms.     The  process  commences  in  the  skin,  of  which  a 

vin  and  inward  to  the  fat,  muscles  and  even  In. lies.        The 

beyond  the  median  hue  and  even  to  other 

n  the  trigeminal  nerve  usually  precedes  and  accompanies. 


Dwarfism,    Microsmia,  Nanosmia,  Achondroplasia     1177 
(1164). 


Disuse  from  Paralysis. 

Facial  1  temiatrophy. 


1178 
1179 


Lilly  of  the  hones.      The  process  i.-  usually 


v  cause  pressure  symptoms  on  the  nerves  running  through 

I    thus,   common   symptoms.      Lower  jaw    and   extremities 


Facia]  I  [emihypertrophy. 

Hyperostosis  Cranii  or  l.eontiasis  Ossen. 


11S0 
1181 


>rics  of  the  hod>  become  enlarged  and  soft,  hut  the  lower 
■come  Lent  and  bowed  (spondylitis  and  kyphosis).     The 
ted. 

nils  and  feet,  lower  jaw,    and   .-termini,    also  ears,    tongUO, 

I  -hoe-.     Thorax  is  much  enlarged  and  patient  is  "round 
iral  hemianopia,  follow  Pain  in 

trophy  of  the  pituitary   body.      If  the  disease  commences 
isteaii  ..1 

pes  of  the  fori  -a  i  d  ften  enlarged,  as  can  be  shown 

eptii  "i  tuberculous  nature  usually.    Thesymp- 

violcnce.  oven  on  turning  the  patient  over  in  bed.     Borne 
softening  of  the  hone  and  diminution  of  lime  sal' 
•en    variously  named:    osteogenesis    imperfecta,  o 


Osteitis  Deformans.    Paget's  Disease. 


Acromegaly  and  Gigantism, 


I  ragilita    I  Issium.     <  toteopsath]  rosi 


1182 


lis:: 


Hypertrophic  I'ul nary  <  Osteoarthropathy.  1 1 s  i 


liv. 


ire   absent       Pains    in    lee-.      Ataxia    without    paralysis. 

.■inpti.m-        \re\  ll-lo.l.ei  i-un's    pupil    rellex. 

I'am-  in  aim         I'  o  ,1 1        .,f  arm-  (alight  I. 

infill  and  thermic,  with  persistence  <>f  tactile,  sensibility. 

or  other  part  •  nt  i»»l\    hands,  fingers,  i  to  I,  are  not  infre- 
r,  ..i  ob  cure  lignificance  and  are  without  diagnostic  value. 


Arthropathy  of  Tabes  (661  I.    (Charcot's  Discaai        1 186 

l  Kins 

Byring yelia  (562,  603,  1170)      (Fl§«.  24-7.)  "s" 


Localised   Hypertrophies  and  Atrophies,  symmet-     1188 

rioaJ  and  asymmetrical 


CHART  XVII  d 

Ganglionic  Disorders,  Vaso-Motor  Disorders 

<  omprising  Numbers  1128,  L 129  and  l  ill' to  1145  on  left  aide  of  Chan 
and  1191  to  L203  on  right  margin 


101 


DIAGNOSTIC  ANALY 


GANGLIONIC  AND  VASO 


DIAGNOSTIC  SYMPTOMS  AND  TESTS 


rll42 
Parah  I  ii 


1128 

GANGLIONIC 

DISORDERS. 


1143 
Irritative. 


lilt 
Vascular 


11  _".i 

VASO-MOTOB 

DISORDERS. 


1 1  1-', 

Exudative 

Secreton 


ABSTRACT  OF 

Ptosis  "I  eyelid,  although  patient  can  raise  it  perfectly  l>y  an  effort  of  will  fj 
not  dilate  when  shaded, although  it  contracts  briskly  when  eye  is  exposed 
sure  with  retraction  and  lowering  of  eyeball  (enophthalmus).     Intra-oc 

abolished,  flushing  of  skin  and  absence  01  sweat  on  the  affected  side  of  fac( 
third  rib. 

The  symptoms  are  exactly  opposite  to  those  of  paralysis  of  the  cervical  syn 
widening  of  the  palpebral  fissure  (Stellwag's  sign)  and  delayed  d<   ■ 
The  Boston-Kocher's  sign,  an  amplification  of  Graefe's  sign,  may  occur  in 

Exophthalmus,  tachycardia,  goitre,  flushing,  sweating,  tremor,  nervousness, 
ward  (Graefe's  sign),  widening  of  the  palpebral  fissure  (Stellwag's  sign),  thl 
The  d  -ease  occurs  much  more  frequently  in  women  than  in  men  and  althi 

the  cervical  sympathetic  ganglia,  yet  it  is  really  due  to  excessive  secretion 
the  reverse  of  those  of  myxedema  (1163),  can  be  produced  by  the  adrnini 

extirpation  of  the  thyroid. 

Paroxysmal  spasm  or  congestion  of  the  bronchioles,  often  reflex  from   nasal 

nervous  temperament  ot  most  asthmatics,  togetherwith  the  very  rapid  on 
may  be  due  to  a  disturbance  of  the  thoracic  sympathetic.  The  paroxyBn 
prolonged  expiratory  murmur,  make  the  diagnosis  easy.  Asthma  is  assocL 
be  in  part  voluntary,  in  part  reflex;  also  is  usually  associated  with  bronch 

Paroxysmal  attacks  of  coldness  and  pallor  ("dead  fingers,"  "local  syncope" 
of  all  together.  These  attacks  may  last  a  few  minute-  or  hours  and  then 
the  same  parts  become  dusky  blue,  or  purplish  black  ("local  asphyxia  or  c 
This  attack  may  pass  off,  after  several  hours,  with  abundant  sweating,  or 
grenous  and  finally  slough  off.  The  necrosis  does  not  usually  invol 
metrical.  It  is  more  common  in  cold  weather  and  is  often  brought  on  bj 
Hematuria  and  evidence  of  congestion  of  other  internal  organs  may  occur 

Analogous!  to  Raynaud's  disease  is  gangrene  of  extremities  occurring  in  mam 
old  age;  either  without  the  local  syncope  ot  loci,]  asphyxia,  or  with  only  s 

Paroxysmal  attacks  of  formication,   tingling,    numbness  and   other  p 

intervals  and  exclusively  m  women,  They  seem  to  be  brought  on  by  ovei 
cases  during  the  attack  the  skin  becomes  pale  and  blue.      Similar  symptoms 

Paroxysms  of  severe  pain  in  one  foot,  rarely  in  both,  rarely  in  hand-  and  ver 

creased  by  allowing  foot  to  hang  down,  or  by  motion  of  it,  or  by  cold.  Tl 
redness  and  swelling  of  the  whole,  or  part,  of  the  sole  of  foot.     Usually  a 

to  a  simple  va-o-motor  neurosis.      The  neuritis,  when  present,  is  often  a8S0 

Occurs  in  middle  aged  or  elderly  persons  and  is  associated  with  arterial  disease 

walk  and  increases  so  that  walking  becomes  impossible.  It  passes  off  after 
attack  the  feet  are  cold  and  then' is  absent  or  greatly  diminished  pulsation  i 

alcohol  and  tobaCCO  and  injur\  seem  to  he  common  cause-  of  this  condition 
feet.      The  arms  are  rarely  involved. 

In  many  diseases  if  lines  or  writing  lie  traced  on  tin'  skin  with  a  sharp  point,  t 
to  lines  of  bright  redness,  which  persist  for  minutes  or  hours. 

rParoxysmal  attacks  of  localized  edema  of  sub-cutaneous  or  sub-mucuou 

a   few   hours  or  days.      The  extent   of  the  edema  varies  greatly.      I' 
!      extremity,  or  even  more.      It  ma\  cause  death  when  occurring  in  the  larynx 
-ure.      They  occur  in  hysteria  and  are  usually  associated  with  a   neiiiasihei 

ociated  with  symptoms  of  digestive  disorder,  thej  an'  called  urticaria 

cept   the  itching.      The  disease  often  show.-  a  strong  heredity  ami  at  timet 

Edema  of  the  lege,  unilateral  bet ling  bilateral,  bad  heredity.    The  edema  i 

being  a  sudden  demarcation  at  the  level  of  the  joint,     The  edema  may  be  ai 

Some  cases  present  paroxysmally  or  constantly  a  profuse  -wealing,  usually  loca 


OF  SYMPTOMS 


OTOR  DISORDERS 
fMPTOMS 


l>I  VGXOSIS 


ido-ptoeis).     Contraction  of  pupil  (myoeis),  which  does      Paralysis  of  Cervical  Sympathetic. 
liulit  and  on  convergence,     narrowing  of  palpebral  fis- 
t<-ri^i< >n  diminished.     The  cilio-epinal  reflex    3353  is 
d  also  mi  aide  of  neck,  or  of  arm  and  thorax  above  the 


ll'.tl 


lulu       Dilatation  of  |iu|nl  (mydriasis),  exophthalmic, 
■r  eyelid  when  eye  is  turned  downward    I  ri 
-■■  ami  in  exophthalmic  goitre  (1 L93 

■  i-iii  ot  upper  eyehd  when  eye  \i  turned  down« 

and  systolic  murmur  in  vessels  of  neck  ami  in  thyroid. 

•  it  it-  symptoms  may  In-  referred  i<>  disorder  of 

mid  gland.     Many  df  n-  symptoms,  which  are 

ti.m  df  thyroid  gland,  and  the  disease  '-an  In-  cured  by 


Irritation  of  Cervical  Sympathetic. 


Exophthalmic  Goitre. 


Freedom  from  symptoms  in  the  interval.    The 

and  cessation  of  tin- attack,  indicates  that  the  disease 

ol  dyspnoea,  with  the  abundant  drj  rale-  ami 

with  strong  contraction  of  tin-  diaphragm,  which  may 


\stlima     617). 


tingli  il;  of  fingers  or  toes  or  tip  of  nose  or  of  eat  -  oi 
iff,  or  may  In-  followed  byan  attack,  in  which 
from  congestion.      Tin-  is  associated  with  pain. 

'I    t  Ik-mi.   may  liccomc  gan- 
be   cyanotic  .ilea.        I  '  i      usually   svm- 

hands  iii  cold  water,  or  by  working  with  hand-. 

•  e-k- 

iioiii  childhood  to 
indicati  conditions  in  -ome  of  the  cases. 

i  Angei  occur  at  irregular 

k   ami  by   having  the  hands  in  cold  water       In  some 

occur  in  tin-  ■  romegaly    1 183 

I  ice.   last  inn  a  feu   minutes  "i  a  few  hours,  m- 

am.  except  iii  the  earliest  attacks   is  accompanied  bj 

only,  ami  i-  generally  due  to  a  net 
•  I  with  atheromatous  artei 

ul  cramp  occur-  in  mi  rfter  a  Bhort 

•  to  return  if  walking  i-  re-uined.      Dunn-   the 

■  i-  pedi    oi  posterior  tibial  artery,     Syphilis, 
infrequent!)  pre  'odes  ■-•  ingrei f  the 


Raynaud's  Disease,   Symmetrical  Gangrene    Mill  .     1195 


I'amilx  i  iangrene 


\i  i < i|>:u i —i  besia. 


I  i\  thromelalagia    1010) 


Intermit  tent    Limping 
Vngio-Sclerotica    554 


[ication      Dyabasia     1199 


bul    i  change      Dermographia  (326, 1167). 


I  _'l  N  I 


iher  white  or  red,  lasting       tape-Neurotic    Bdema    and     Urticaria.      1167),     1201 
■hall  inch  in  din  ijun, 

inditioi  i  in  clor   itch  and 

Iraw  ii  between  the  two  di 


I"   limited  above  bj  the  ankle,  knee  "i  groin;  then 


\hlrm     oi   '  '  phoden 

Hyperhidi  ive  Sweating 


CHART  XVIII 
Syphilis  of  the  Nervous  System 

I  !omprising  Numbers  1205  to  1217 


DIAGNOSTIC  SYMPTOMS  AND  TESTS 


DIAGNOSTIC  ANAI 
SYPHILIS  OF  THf 


1205 

S"5  I II I  LIS  01   THE 

NERVOUS  SYSTEM. 

Hi-  tory  of  personal,  or  hered- 
itary, syphilis.  Physical  ev> 
dence  of  syphilis;  such  as 
W  assei  1 1 1 : 1 1 1 1 1  reaction,  a 
chancre  or  its  scar,  indu- 
ration, mucuous  patches,  a 
syphihtic  rash  or  ite  copper 
colored  scars,  hazy  cornea, 
notched  teeth,  furrows  about 

angle  of  mouth,  saddle  nose, 

ptosis,  iritis,  enlarged  glands, 
pi  i  iosteal  nodes,  etc. 


'Syphilitic  Nervous  Diseases. 

Symptoms  of  syphilis  of  the 
nervous  system  are  very 
variable  from  day  to  daj 
transitory  and  manifold. 
They  consist  of  paresis,  rather 
than  of  complete  paralysis. 
They  usually  show  rapid  im- 
provement under  K.I.  and 
Hg.  or  Salvarsan.  Nocturnal 
headache  is  common,  as  are 
also  the  Argyll-Robertson's 
pupillary  reflex,  unequal  pu- 
pils and   optic  neuritis. 


i  lerebral  symptoms. 

Although  these  symptoms 
can  lie  divided  into  several, 
more  or  less  well  defined, 
groups,  yet  a  combination 
of  several  or  all  of  the  lesions, 
in  varying  intensity,  is  not 
infrequent;  so  that  a  combi- 
nation of  the  symptoms  of 
several  or  all  of  the  groups 

may  be  present   in  one  case. 

Pure,  uncomplicated  cases  "i 

each  type  are,  however,  com- 
monly met  with. 


Spmal  symptoms. 

i  Both  forms  of  spinal  syphilid 

may  occur  together  i 


( lerebral  and  spina 
symptoms. 


'Little  or  no  ivii 
in  cerebro-spinal 
lumbar  puncture. 


( llobulin  and  d 

"i  \  tOSis   is  foil 

spinal     Moid 

(jiuneture. 


eeid. 
lid  ii 
from 


No  globulin  and  lit 
lymphocytosis  I'mni 
cerebro-spinal  fluid 
lumbar  puncture. 


( llobulin  ami  decide 
oeytosis  found  in 
spinal  fluid  from 
puncture. 


( llobulin  and  decide 
oeytosis  in  cerebro 

fluid. 


1 ■'''    Peripheral   symptoms.      Wassermann  reactio 

blood.   Normal  eerebi 

Hind. 


Post-,    or    Met.,-,    syphilitic    ("Cerebral  symptoms. 

nervous  di-ease. 

spmal  symptoms. 


I  increased    lymphoqj 
fcerebro-spinal  fluid. 


SIS  OF  SYMPTOMS 


ERVOUS  SYSTEM 


from 


Vlliph- 

rebro- 

imliar 


ABSTRACT  OF  SYMPTOMS 

Symptoms  of  cerebral   tumor  (507,  636).     Other  syphilitic 

ptoms  may  be  present.     Rapid  course  with  irregular 

remissions  and  intermissions.    The  symptoms  of  cerebral 

compression  are  much  less  pronounced  than  in  non-syphilitic 

tumors.    Very  amenable  to  anti-eyphilitic  treatment. 

Symptoms  of  cerebral  thrombosis  (506).  The  attacks  occur 
rather  early  in  adull  life.  There  are  manj  prodromata 
Nocturnal  headache  is  common.    The  p  noderate 

in    degree,    variable    in    intensity    and    often    temporary 
Mental  derangements,  often  in  the  form  of  trance-liki 
frequently  occurs.     Branches  of  the  basilar  arterj  are  in- 
volved most  frequently,  and  the  attack  often  occurs  during 
sleep,  or  without  coma  during  the  day. 

^Symptoms  of  cortical  irrita- 
tion (Jacksonian  epilepsy, 
local  headache  and  tender- 
id  paralysis  of  cortical 
function  mono- 
Mental  de- 
rangement   is  comi and 

often    takes    the    form    of 
pseudo-paresis),  but 
ible  to  anti-syphilitic 
treatment. 


Symptoms  of  meningitis  (590, 
hi  is*,  which  ma}  be  very  slight 
and  very  variable.  \\  ill, 
severe  headache    noi 

there    may    |„ 

and  vomiting.     Little  or  no 
elevation  of  temperature  or 
So 
tuberculi 

dence  of  tuberculosis.     This 
hildren. 


mptoms    of    cortical 
a     or     paralysis     ol 
functions,    r 
"i  cranial  nerves  (e  | 

'i oulo-motoriue 

■  irregular  distribu- 
tion and  m  varying  degree. 
Drowsiness  and  stupor  are 
.common, 

,,r  do    f^ynptoms  of  Brown-Sequard's  paralysis,  or  later  of  para- 
plegia    II.'.  509,  840,  981 

ptonru  of  myelomalacia     185,  513-4,  517-8,  549-50). 
mptoms  of  lateral  scl 


mpn- 

mlial 


Symptoms  of  spinal  menin  pachymeningiti 

Rigiditj    of   back.     Girdle   pain 

radiating   pains,   exaggerated    reflexes    in    legs      S i 

theBe  '"'-'-   present    the   symptoms  of   progressive  spinal 

mils.  ' 


A   combination   ol    the 


'-  mptuim     12084,    1213     in 
intensity        \    clinical    picture 
compri  pina)  symptom    and  presenting 

hich   arc   impo  Bible    to   describe   in    a 

leu    WOI 


DIAGNOSIS 
Isolated  Cerebral  Gumma 


Cerebral  Syphilitic  Endarteritis     1207 
and  Thrombosis 


Syphilitic    Meningitis   of   Con-     1208 
verity  of  Brain. 


Syphilitic  Meningitis  of  B 
Brain,    including    K 
I  liscase. 


L209 


Isolated  Spinal  I  .11111111:1 


Spmal    Syphilitic    Endarteritis 
and  Thrombosis. 

I. ii.'s    Syphilitic    Lateral 

IOSIS 

Syphilitic    Meningitis   of   Cord 

and  ..I    \.  1  \  e  Root  \lniiii- 

go-myelitis,    Pachymeningitis 
<  lervicalis       ll\  pertrophica.J 


1210 
L211 
1212 

1213 


the      Sympton 
pinal 


■   I,  940-8 


1  loi 
nptotns  of  be tor  atari  i    661 


<  'erebro-Spinal  83  philis 


Syphilitic  Neuritis 


Looomotoi      Marin       1  ibei 

I'.c         '. 


1215 


i.'i.. 
IJI7 


CHART  XIX 
Abnormal  Cerebro-Spinal  Fluid 

Comprising  Numbers  1220  to  1242 


•jii: 


L223 

Leucocytosis 


1221 

Butyric    acid    tesl 
positive. 


l220 

\n\m;.\i  \i. 
I  EREBRO- 
8PINAL 

I  l.i  ID 


1224 

Lymphocytosis. 


L222 

Butyric    acid    tesl 

negative. 


DIAGNOSTIC  ANA1 


ABNORMAL  CER1 


Weichselbaum's  diplococcus 
intra-cellularis  meningitidis 
or  rarely  Pneumococcus 

Weichselbaum's  diplococcus. 

I'ncuiiineoccus,  Pfciffcr's 

bacillus.  Streptococcus, 

Staphylococcus,  Typhoid 
bacillus.  Bacterium  coli,  etc 

Tubercle  bacillus.  "i 


(■Tubercle  bacillus 


TESTS  AND  I> 

Fluid  im.-iv  be 
Tension  mere 


Wassermann 
tive. 


•Iloll       posl- 


\\  assei  111:11111    react  ion    nega- 
tive. 


1225 

No  Lymphocytosis 

or  Leucocytosis 


No  bacteria  and  \\  ossermi 
negat  ive 


Fluid    usual!} 
under  high  tei 


Fluid  usually 
cate    coagulu 

liii;li  tension. 


Fluid    clear 
bacteria. 


Tension  is  us 
but  not  very 


Fluid    cIcm 
tension;  in 

bloody 


5IS  OF  SYMPTOMS 


*0-SPINAL  FLUID 
tNOSTIC  8IGNS 


DIAGNOSIS 


i  or  cloudy.      Occurs   in  epidem-      Symptoms  of  epidemic  Cere-      Epidemic  Cerebro-epinal  Meningitis.      1226 
1  usually.  bro-spinal   meningitis    (591). 


loudy      and        <  Iccurs  .-( ior;n I- 

ically. 


Symptoms     of     sporadic     or       Sporadic  Purulent  Meningitis. 
purulent  cerebro-epinal  men- 
ingitis (592). 


1227 


r  with  deli- 
and    under 


I  Acute  course. 


(  'limine  course. 


f  Acute,  or  sub-acute  Tuberculous 
Ma 


Symptoms     of     tuberculous    ■  Meningitis, 
meningitis   59 

Chronic  Tuberculous  Meningitis 


[Tremor  and  mental      Sympl b  of  Paresis  (1104).      Paresis. 

symptoms. 


free    from    .  Ataxia 


Symptom.-  of  Tabes  (661 1.         Tabes. 


Symptoms  not   typically  characteristic  of  paresis      Cerebro-spinal  Syphilis  (1208-9,  1213- 
or  tabes,  being  due  to  a  cerebro-spinal  menin-  14). 

*■    gitis. 

Motor  paralysis.  Symptoms  of   acute   anterior       Acute  Anterior  Poliomyelitis. 

poliomyelitis    i  195).      I  Figs. 
26-7 


1228 

1229 
1230 

1231 
1232 


Herpetic  rash 


Symptoms  of   herpes   Boater      Herpes  Zoster 
- 1  166). 


l-pid.i High      Symptoms  of  Typhus. 

fever. 


T\  phus  Fevei 


Choked  disc  usually       Symptoms    of    cerebral    or      Tumor 
present  spinal  tumor    507,  678,  587). 

Symptoms    of    cerebral    or      Abscess 

spinal  abscess  .Mis,  ,"i7s,  587). 


t  'lioked    disc    mi 

I.,    pn    cut 


Headache 

Apo w 


Sj  mptoms  of  hydrocepl 

1 1  ill.  no:,,  966).  ' 


this      Hydrocephalus. 


Symptoms  of  serous  menin-      Serous  Meningiti 
tin-  (594 

Symptoms    of    cerebral    or      He rrh 

spinal  hemon  li 

i' i 


A U him i.  r ,  [examination    of    the    nunc      I  remia 

albumen  and  casts 
1  !•  mi,  headache,  dj  spnoi  n 
etc    usuallj  present 


Anemia 


I  Examination    -leu     anemia,       Anemia 
pallor,   etc  .  or  anii,'   infec- 
tions, "i    tome   similai    con 
ditions 


vs.\:, 
1236 
1237 
1238 
1239 
1240 


PART  III 


LOCALIZATION 
OF 

LESIONS  WITHIN  THE  NERVOUS  SYSTEM 

BY 

A  CONSIDERATION  OF  THE 

PARALYTIC  AND  IRRITATIVE  SYMPTOMS 

RESULTING  FROM  THEM 


CHART  XX 

Spinal  Localization 

Comprising  Numbers  1250  to  1267 


90S 


TABLE  OF  SYMPTOMS  IN  TRANSVERSE  LESIONS  OF  THE  CORD 


Modified  from  Wichman 


Segment 


Involved 

Reflex 

Sensory 

Motor  Conditions 

Conditions 

Conditions 

,     Anesthesia 

In- 

with a  zo^e  of 

creased  hyperesthesia 

_x 

in 

surrounding 
it  or  limiting 

Actions  lost  or 

partia 

Paralysis 

Paresis 

impaired 

Absent 

lesions 

it  above 

1250 

None. 

Coccygeus. 

Elevation  of 

Anal. 

None. 

Skin  over  sac- 

V 

coccyx. 

rum  and  anus. 

Sacral 

1251 

Coccygeus. 

Levator  ani. 

Elevation  of 

Erection 

None. 

Slightly  larger 

IV 

coccyx. 

of  penis 

area  than  above 

Sacral 

Sphincter  ani. 

Elevation  of  anus. 

dimin- 

extending over 

Detrusor  urinae. 

Sphincter  ani. 

ished. 

inner  portion 

Transversus  perinei 

.  Ejection  of  urine. 

of  gluteal 

Erector  penis. 

Vaginal  constriction 

. 

region. 

Compressor  urethrae. 

r  Sphincter  ani 

Rectum. 

Defecation  dis- 

Ejaculation 

As  above,  and 

Levator  ani. 

turbed. 

lost. 

perineum,  gen- 

Detrusor 

Retention  of  urine, 

Erection 

itals  and  upper 

1252 

urinae. 

later  followed  by 

diminished. 

part  of  inner 

III    - 

Transversus 

dribbling. 

Tendo- 

surface  of 

Sacral 

perinei. 
Erector  penis 
Compressor 
■  urethrae. 

Ejaculation  lost. 
Erection  possible 

Achillis. 

thighs. 
(Testicle  sensi- 

but paretic. 

tive  to 

pressure.) 

f  Sphincter  ani 

Pyriformis. 

Outward  rotation 

Ejacula- 

None. 

As  above,  and 

Levator  ani. 

Obturator  internus 

of  thigh. 

tion. 

the  posterior 

Gemellus  superior. 

Retraction  of  thigh 

Erection. 

surface  and 

Gluteus  maximus. 

Flexion  of  knee. 

Plantar 

outer  surface 

Biceps  femoris. 

Plantar  flexion  of 

weakenec 

of  thighs. 

1253 

Gastrocnemius. 

foot. 

n   H 

Soleus. 

Standing  on  the  toes 

Sacral 

Tibialis  posticus. 

Raising  inner  margin 

Detrusor  urinae 

of  foot. 

and  other 

All  the  small  mus- 

Defecation and 

muscles  as  in 

cles  of  foot. 

Retention  of  urine 

.  3d  sacral. 

as  in  3d  sacral. 

210 


TABLE  OF  SYMPTOMS  IN  TRANSVERSE  LESIONS  OF  THE  CORD  (Continued) 


Modified  from  Wiehman 


Segment 
Involved 


Motor  Conditions 


Reflex 
Conditions 


1254 
I 

Sacral 


Paralysis 


Muscles  of 
anus. 

Muscles  of 
bladder. 
Muscles  of 
genitals. 
Piriformis. 
Abductor 
hallucis. 
Flexor 
hallucis 
brevifl. 
1-1 V  dorsal 
interossei. 
I-III  plantar 
interossei. 
111-IV  lum- 
bricales. 
Abductor 
minimi 
digiti. 
<  )|>ponens 
I.  minimi  digiti. 


Paresis 


Actions  lost  or 
impaired 


Absent 


Sensory 
Conditions 
Anesthesia 
with  a  zone  of 
creased  hyperesthesia 
in         surrounding 
partial     it  or  limiting 
lesions         it  above 


In- 


Retention  of  feces. 

Retention  of  urine 

or  dribbling.  Plantar      None. 

Erection  and  ejacu-  weakened. 

lation  impossible.      Achilles- 


Gluteus  maximus. 

Obturator  internus. 

Gemellus  superior. 

Gluteus  mediae. 

Gluteus  minimus. 

Biceps  femoris. 

S(  'in  i  -  membranosus 

Semi-tendinosus. 

Popliteus. 

Gastrocnemius. 

Soleus. 

Tibialis  posticus. 

Peroneus  longus. 

Peroneus  brevis. 

Flexors  of  toes. 

Extensors  of 

toes. 


tendon 

reflex. 

Ejaculation. 

Erection. 

Micturition. 

Defecation. 

Gluteal. 


1  •_».-.:. 

Y 
Lum- 
bar 


Muscles  of  anusGemellus  superior. 


and  rectum. 

I  is  of 
Madder. 
Muscles  of 

genitals. 
Pyriformis. 
Biceps 
femoris. 
Flexors  of 

Peroneus 

longus. 

Peroneus 
brevis. 


Gemellus  inferior. 
Gluteus  medius. 
Gluteus  minimus. 
Semimembranosus 

Semi-tendinosus. 
Gluteus  maximus. 
Tensor  fasciae 
femoris. 
Gastrocnemius. 
Soleus 

Extensors  of  toes. 
Tibialis  anticus. 


Outward  rotation 
of  thigh  im- 
paired. 

Internal  rotation 
impaired. 
Flexion  of  knee 
difficult. 
Plantar  flexion  of 
foot. 

Raising  inner  mar- 
gin of  foot. 
Raising  outer  mar- 
gin and  dorsal 
flexion  of  foot. 
Flexion  and  extension 
of  toes,  adduction  of 
gnat  toe,  abduction 
of  little  toe,  etc. 


Defecation. 

Micturition  delayed, 
dribbling. 

Erection  and  ejacu- 
lation impossible. 
(  hit  ward  rotation 
of  thigh  very 
difficult. 
Inward  rotation 

impaired. 
Flexion  of  knee 
difficult. 

Retraction  of  thigh    ('.luteal 
very  difficult. 

Flexion  of  fool 
barely  possible. 
Flexion  of  toes 
impossible. 
Extension  of  toes 

weak,  except    great 
toe,  which  may  he 
dorsallv  flexed. 
Raising  inner  margin 

df  fool  difficult. 

Raking  outer  mar- 
gin of  foot  im- 

I  ile. 


As  above,  and 
a  strip  on 
posterior  and 
outer  surface 
of  lower  legs 
and  of  dorsum 
of  foot  and 
especially  of 
toes. 


Ejacu- 
lat  on. 


Plan- 
tar. 


A<  above,  and 

hack  of  thighs 


Erection.  Tendo-  and  legs  and 

Achil-  inner  and  outer 

lis.  margin  and 

Micturition.  sole  of  feet. 

Defecation. 


-Ml 


TABLE  OF  SYMPTOMS  IN  TRANSVERSE  LESIONS  OF  THE  CORD 

Modified  from  Wichman 
Segment 

Involved  Reflex 

Motor  Conditions  Conditions 


(Continued) 


Paralysis  Paresis 

Muscles  of  rec- 
tum and  anus. 
Muscles  of 
bladder. 
Muscles  of 
genitals. 
Obturator 

internus.  Obturator 

Pyriformis.  internus. 

Gemelli. 

1256  Gluteus 
IV       medius. 

Lum-      Gluteus 
bar         minimus. 

Gluteus 

maximus. 

Biceps 

femoris. 

Semi- 
membranosus. 

Semi- 

tendinosus. 

Popliteus. 

Gastrocne- 
mius. 

Soleus. 

Flexors  of 

toes. 

Extensors  of 

toes. 

Peroneus 

brevis. 

Peroneus 

longus. 

Tibialis 

anticus. 

Muscles  of         Vastus  internus. 
anus,  bladder  Rectus  femoris. 
and  genitals.     Crureus. 
Outward  ro-     Adductors  of  thigh, 
tators  and         Flexors  of  thigh 
thigh.  at  the  hips. 

Inward  rota- 
tors of  thigh. 

1257  Retractor 
III        (flexor)  thigh. 

Lum-      Flexors  of  knee, 
bar         Plantar  flexors 

of  foot. 

Flexors  of  toes. 

Extensors  of 

foot. 

Vastus  externus. 


Rectus  femoris. 
Vastus  externus. 
Vastus  internus. 
Adductor  magnus. 
Adductor  brevis. 
Adductor  minimus. 
Gracilis. 


Actions  lost  or 
impaired 


Absent 


Sensory 
Conditions 

,      Anesthesia 

In-      with  a  zone  of 
creased  hyperesthesia 
in  surrounding 

partial     it  or  limiting 
lesions        it  above 


Defecation,  with        Patellar     Plan- 
fecal  incontinence,     may  be      tar. 
Micturition,  with       wanting, 
dribbling. 

Erection  and  ejacu- 
lation impossible. 
Outward  rotation  of 
thigh  weak. 
Inward  rotation 
impossible. 
Retraction  of  thigh 
impossible. 
Flexion  of  knee 
lost. 

Plantar  flexion  of 
foot  lost. 

Flexion  and  exten 
sion  of  toes  lost. 
Raising  outer  mar- 
gin of  foot. 
Raising  inner  mar- 
gin. 

Extension  of  thigh 
weak. 
Adduction  difficult. 


All  movements  of      Patellar     Ankle- 
legs  are  lost,  except  and  clonus 
that  extension  of       cremas-     may 
legs  is  barely  pos-      teric.          exist. 
sible  and  that  the 
thigh  can  be  flexed 
on  body  by  the 
psoas  and  iliacus. 
Defecation  and  mic- 
turition are  de- 
stroyed. 
Urine  and  feces 
dribble  and  cannot 
be  retained. 


212 


As  above,  and 
inner  side  of 
lower  legs  and 
dorsum  of  feet, 
and  strip  on 
outer  posterior 
surface  of 
thighs. 


As  above,  and 
whole  of  legs 
except  a  tri- 
angular area  on 
front  of  thigh 
with  base  at 
Pou  part's 
ligament. 


TABLE  OF  SYMPTOMS  IN  TRANSVERSE  LESIONS  OF  THE  CORD     (Continued) 


Modified  from  Wichman 


Segment 
Involved 


Motor  Conditions 


Paralysis 


Paresis 


1258 

Paralysis  of      ] 

11 

all  muscles 

Lum- 

of lower 

bar 

extremity, 

except  psoas. 

1259 

Total  paralysis 

I 

of  whole  lower 

Lum- 

extremity, 

bar 

psoas  included. 

Paralysis  of 

lower  extrem- 

ity, and  gluteal 

1260 

region. 

XII 

Paralysis  of 

to  III 

abdominal  and 

Dor- 

and dorsal 

sal 

regions,  gradu- 

ally added  as 

the  site  of  the 

lesion  ascends. 

1261 

As  in  3d 

II 

dorsal. 

Dor- 

sal 

1262 

All  mil 

1 

of  trunk  and      1 

Dor- 

lower ex-         1 

sal 

tremitiee. 

Psoas. 


;s 

Reflex                Senbobt 
Conditions          Conditions 

*                        Anpsfhesin 

Absent 

Patellar, 
Achilles, 
and 

cremas- 
teric. 

In-       with  a  zone  of 

creased    hyperesthesia 

in         surrounding 

Actions  lost  or 
impaired 

Complete  paralysis 
of  legs,  rectum 
and  bladder. 

As  above. 

partial     it  or  limiting 
lesions         it  above 

Achil-    Whole  of  legs 
les          and  pelvis, 
may       (Testicles  not 
be  in-         sensitive  to 
creased,     pressure.) 
Plantar. 

Cremas-     Patel-    As  above,  and 
teric  and   lar  ab-  groins  and  front 
Achilles,    sent  or  of  scrotum  and 

in-  penis. 

creased. 


Epigas-      Patel-    As  above,  and 
trie  and     lar,         a  band  running 
umbical     ere-        around  body 
reflex.        mas-      about  two  seg- 
terie,     meiits  below 
Achil-    the  one  in- 
les  and  volved  and 
Plan-     limited  above 
tar.         by  a  narrow 

zone  of  hyper- 
esthesia, 


All  below  All  As  above,  and 

losl  in        subja-  a  strip  on  the 

complete  oeni  inner  side  of  the 

division     re-  upper  arms. 
of  conl.     flexes. 

Flexion  of  fingers.  Asal»>ve  and  weak-  Oculo-  All  As  above,  and 
Muscles  of  the  little  oesa  is  flexion  of  papillary  Bubja-  a  strip  on  the 
finger.  fingers.  symp-       sent       inner  side  of  the 

1  1 1  and  IV  inter-        Pronation  dis-  toins.  re-  forearms. 

ossei,  turbed.  All  below  Sexes. 

Lumbric  losl  in 

Pronator  quadratua.  complete 

Lower  part  of  pec  division 

totalis  major.  of  cord. 

Lower  pan  of  pea 
toralil  minor. 


As  above,  and 
paralysis  of  mus- 
cles of  respiration 
causes  diaphragm- 
atic breathing  and 
dyspnoea. 


As  above. 


.- 1 3 


TABLE  OF  SYMPTOMS  IN  TRANSVERSE  LESIONS  OF  THE  CORD     (Continued) 


Modified  from  Wichman 


Segment 


Invol 

VED 

Reflex 

Sensory 

Motor  Conditions 

Conditions 

Conditions 

,      Anesthesia 

In- 

with a  zone  of 

creased      hyperesthesia 

A 

in 

surrounding 
1       it  or  limiting 

Actions  lost  or 

partia 

Paralysis 

Paresis 

impaired 

Absent 

lesions           it  above 

Paralysis  of 

Flexors  of  the  lit- 

As above. 

Oculo- 

All 

As  above,  and 

muscles  of 

tle  finger. 

pupillary 

below. 

the  fingers, 

trunk  and 

Opponens  minimi 

symp- 

except volar 

lower  extrem- 

■ digiti. 

toms. 

surface  of  the 

ities. 

Flexor  subl.  digi- 

thumb  and  the 

Abductor  of 

torum. 

ulnar  surface 

little  finger. 

Flexor  profun.  digi- 

All  below 

of  the  little 

Adductor  of 

torum. 

lost  in 

finger. 

1263 

thumb. 

Flexor  carpi  ulna- 

complete 

VIII 

Flexor  of  the 

ris. 

division 

The  cervical 

Cer- 

little finger. 

Extensors  of  the 

Hand  weak. 

of  cord. 

sensory  nerve 

vical 

Opponens 

thumb  and  fingers. 

roots  supply  the 

minimi  digiti. 

Triceps  (slight). 

Extension  of  arm. 

same  area  of  the 

Ill  and  IV 

Latissimus  dorsi 

Int.  rotation  and 

skin  in  common, 

interossei. 

(lower  part). 

retraction  of  arm. 

especially  in  the 

Lumbricales. 

Pectoralis  major. 
Pectoralis  minor. 
Scalenus  medialis. 
Scalenus  posterior. 

Adduction  of  arm. 

hands  and  fin- 
gers.  Hence  the 
anesthesia  is 
slight  and  un- 
certain. 

Lower  ex- 

Extensors, 

As  above  and 

Arm 

All 

As  above,  and 

tremities  and 

Flexors 

Hand  very  weak. 

reflexes. 

below. 

most  of  the 

trunk. 

and 

(Winged  scapulae.) 

Forearm 

hands  and  a 

Flexor  pro- 

Abduct ins 

Retraction  and  in- 

reflexes. 

small  strip  on 

fundus  digi- 

of  thumb. 

ward  rotation  of 

Palmar 

the  anterior, 

torum  (ulnar 

Extensor  indicia. 

arm. 

reflex. 

another  on  the 

side). 

Extensors  of  the 

posterior,  sur- 

1264 

Flexor  carpi 

fingers  (movements 

face  of  the 

VII 

ulnaris. 

barely  possible). 

All  below 

forearm. 

Cer- 

Small hand 

Supinator  longus. 

lost  in 

vical 

muscles. 

Biceps  (very  slightl; 

y 

complete 

Pronator 

paretic). 

cord 

quadratus. 

Triceps. 

Pectoralis  major. 
Serratus  magnus 
(slight). 

Latissimus  dorsi. 
Teres  major. 

division. 

214 


TABLE  OF  SYMPTOMS  IN  TRANSVERSE  LESIONS  OF  THE  CORD  (Continued) 


Modified  from  Wichman 


Segment 


NVOLV 

ED 

Reflex 

Slnsory 

Motor  Conditions 

Conditions 

Conditions 

A 

Anesthesia 

In- 

with a  zone  of 

creased 

1    hyperesthesia 

A 

in 
partial 

surrounding 

' 

Actions  lost  or 

it  or  limiting 

Paralysis 

Paresis 

impaired 

Absent         lesions 

it  above 

Muscles  of 

Coraco-brachialis. 

As  above  and 

Arm           All 

As  above,  and 

lower  extrem- 

Biceps. 

movements  of  fin- 

reflexes,    below. 

whole  of  hands 

ity  and  trunk. 

Brachialis  anticus. 

gers  and  thumb 

Extensor 

and  fingers  and 

Muscles  of 

Supinator  brevis. 

impossible. 

forearm 

radial  side  of 

fingers  (in- 

Deltoid. 

Extension  of  fore- 

reflexes. 

forearm. 

cluding  thumb)Scaleni. 

arm. 

1265 

and  hand. 

Splenii. 

Flexion  of  forearm 

VI 

Triceps. 

Deep  head  and 

weak. 

All  below 

Cer- 

Pectoralis 

neck  muscles. 

Supination  very 

lost  in 

vical 

major. 

weak. 

complete 

Latissimus 

Adduction  of  arm 

cord 

dorsi. 

and  inward  rota- 

division. 

Teres  major. 

tion. 

Infraspinatus. 

Adduction,  retrac- 

Serratus 

tion  and  external  re 

i- 

magnus. 

tation. 

"Winged"  scapulae 
Raising  of  arm. 
Rotation  of  head. 
Fatal  in  a  few  days 
or  weeks. 

Muscles  of 

Levator  anguli 

As  above  and 

Scapular  All 

As  above,  and 

lower  extrem- 

scapulae. 

shoulders  raised 

and            below. 

whole  of  arms. 

ities  and 

Scaleni. 

with  difficulty. 

tendon 

except  tip  of 

trunk. 

Diaphragm  (be- 

Rotation and  flex- 

reflexes of 

shoulder. 

1266 

All  the  mus- 

cause of  filaments 

ion  of  head. 

paralysed 

V 

cles  of  the 

from  V  cervical  scg 

;-  Dyspnoea. 

muscles 

Cer- 

arm, fi 

meat  to  phrenic 

in  arms. 

vical 

hand  and  fin- 
gers; even  th( 

nerve),  <>r  spread  0 
•  injury  from  6th 

f 

deltoid, 

to  ith  oervioal 

All  below 

loraco- 

segment . 

Fatal  in  a  few 

lost  in 

brachialia  and 

Trapezius  and 

hours  or  days. 

complete 

braohialis 

Bterno-cleido 

cord 

antirus. 

toid  are  intact. 

division. 

I  leep  oervi- 

oal  Mm  dee. 

IntfP 

I2<i7  Total  oroes-lesioni  from  the  fourth  oervioal  segment  upward  are  rapidly  fatal,  because 
IV  l  of  complete  paralysis  of  the  diaphragm  and  interoostals, 
Cer- 
vical Total  oross-lesioni  of  the  brain-stem  are  rapidly  fatal  for  the  same  reason, 


'i:, 


CHART  XXI 

Cerebral  Localization 

Comprising  Numbers  1268  to  1286 


217 


CHART   XXI  a 

Cerebral  Localization  in  the  Medulla  and  Pons: 
Ganglia  at  Base 

Comprising  Numbers  L268  and  1269 


219 


TABLE  OF  SYMPTOMS  IN  T 


Seat  of  Lesion 

121  IS 

Lesion    involving   lateral   half   of   the  Medulla 
Oblongata. 

Babinski  and  Nageotte's  Bulbar  Syndrome  (437). 

Rare  because  of  the  small  transverse  area  of  the 
medulla. 

Thrombosis     of     Posterior     Inferior    Cerebellar 
Artery  causes  very  similar  symptoms. 
(Figs.  21-3.) 


Confined  to  the 
bridge    portion. 


1269 

Lesion  in  lat- 
eral half  of  the 
Pons  Varolii. 
(Fig.  20.) 


Lesion  in 

Lower 

(Caudad) 

Third. 


( 'ontined  to  the 
tegmentum. 


Lesion  in 

Mid. lie  and 

I  < 

(Cephalad) 
Third. 


I  'unfilled  to  the 

bridge  portion. 


(  '. ,1,1,1m, |    |n    |||, 

tegmenl  tun. 


Paralysis  of 
Motion 

( In  issed  paralysis:  hemi- 
plegia alternans  hypoglos- 
siea.  Homolateral  half  of 
tongue,    diaphragm    and 

VOCal  cord,  contralateral 
arm  and  leu.  In  some 
cases    arm    and    leg    may 

be  paralysed  on  both 
sides,  but  not  equally  so. 
Extremely  rarely  leg  on 
one  side  and  arm  on  the 
other  are  paralysed. 

Crossed  paralysis:  hemi- 
plegia alternans  facialis 
Muscles  of  expression  of 

homolateral  half  of  face 
anil  the  external  rectus 
at  times,  and  contra- 
lateral arm.  leg  and  half 
of  tongue  i  Millard-Cub- 
ber's  syndrome — 139). 

Muscles  of  expression  of 

homolateral  half  of  face 
and     of     external     reclus 

i  Foville's  paralysis).  Con- 
tralateral arm  and  leg 
may  lie  slightly  involved. 


Complete       contralateral 

hemiplegia. 


Conjugate    deviation    of 

eyeballs  toward  the  side 
of  the  lesion.  May  be 
complete  hemiplegia  of 
slight  degree  from  pres- 
sure. 


Paralysis  of 
Sensation 

Taste  in  posterior  part 
of  homolateral  half  of 
tongue.  All  forms  of 
sensation  in  pharynx  and 

throughout  the  respira- 
tory tract.  Analgesia 
and  thermic  anesthesia 
of  homolateral  half  of 
face  and  contralateral  half 
of  body.  Anesthesia  of 
one  side,  or  of  both 
sides  of  the  body. 

None,      unless  indirectly 

from    pressure  and     then 

contralateral  hemianes- 
thesia. 


Contralateral  hetnianal- 
gesia  and  thermic  an 
ethesia  and  at  times  hemi- 
anesthesia. Anesthesia, 
and  especially  analgesia, 
of     homolateral     half     of 

fad-  (Hemianesthesia  al- 
ternans). Very  rarely, 
deafness,  Rarely  disso- 
ciation of  sensation. 

Usually    of    all    forms    of 

sensation  in  homolateral 
half  of  face.   ( iceasionallj 

also      hemianesthesia      of 

contralateral  half  of  body. 


Paralysis  of   all   forms   of 

sensation  on  homolateral 

hall  of  face.   Contralateral 
heminnalgesia.       May    be 

contralateral      hemianes- 
thesia 


LOCALIZATION 

Action  Lo 
Impair 

Articulation, 
deglutition,       r 
cardiac    action, 

vomiting,   use 
and   of   arms   a 
one  or  both  sidi 


Articulation, 
mastication,    a 

of     homolateral 

lace,    and    of   Co 
arm  and  leg. 


Articulation,  m 
winking.  Muv 
homolateral  hat 


('hewing       and 
articulation.     M 

of    contralateral 

body. 


( Shewing      and 
articulation, 
movement      of 

toward    the   sain 
the    lesion. 


MSVERSE  LESIONS  OF  BRAIN-STEM 


MEDULLA  AND  PONS 


nation, 
ration, 
ighing, 
tongue 
leg  on 


Rbflexes 

Altered 

Tendon  reflexes  increased 
with  Babinski  and  ankle- 
<-l' .tin-  mi  opposite  Bide, 
Cutaneous  reflexes  may 
or  may  not  !»■  increased. 


\  1 1 
( foually  present  - 


Atwia 

Usually  present 

i  both  motor 
and  cerebellar  type. 
Homolateral. 


Ml  SCLB 
Si  MSB 

Usually  lust,  espe- 
cially if  mi  >t  i  ir 
ataxia   be   present. 


Sbcretobi   iMi 

( iiiu.ii  Drsn  mi  u»a  - 

Myosis  :inil  pseudo-ptosi - 
(ophthalmoplegia  sym- 
patbica)  and  salivation 
are  common.  Cheyne- 
Stokes's  respiration 


inking, 
•mei  is 

aJf      Of 

lateral 


Tendon  reflexes  increased 
with  Babinski  and  ankle- 
clonus  mi   opposite   siilr. 

Cutani •    reflexes    may 

01  maj   not  be  incn 


<  ifii'ii  present. 


No  motor,  bul 
there  may  !»■  cere- 
bellar, ataxia. 


Conjunctivitis  is  frequent 
in  eye  of  same  side.  May 
be  :i  tendency  to  fall  «>r 

to  turn  tu  iini-  siilc 
Salivation. 


■:iln  n, 
nt-    Of 


Normal  >.r  slieliiU   exag- 
gerated us  above. 


I  -ii.illv  present . 


I  mall}  present  on 
the  Borne  aide  as 
the  lesion, 


i.'ii   ,ni  i In-  same 
side  as  thr  lesion. 


<  Soniunctivitis  is  frequent 
in  the  eye  of  the  same 
aide     Salivation. 


Tendon  reflexes  incre  ised  I  ifteo 
with  Babinski  and  ankle- 
clonus  "N  the  oppo  !'• 
side,  Cutaneous  reflexes 
may  or  maj  not  l>" 
increased. 


No  motor,  may  It      Normal 
cerebellar,  ataxia 


I  Iceratii t  cornea  maj 

occur    Ma)  be  a  tendency 
i"  fall  "i  turn  i le  sidi 


jugtite 


Normal  or  maj  be 

it«l 


■  liL'liil\       Present 


M:i\  be  motor  ai 

iiTilii-llal   at  \:tl.i 


Lost    "ii   iIh-  sain" 
— i ■  1  < -  as   ill"  lesion. 


Ulceration  of  ill"  <■■  >rnt-:i 
ma]  rarely  occur  \ 
slow  rhj iliini"  tremor  "t 
tin-  arm  and  l"g  of  oppo- 
site side  maj  be  present 


CHART  XXI  b 

Cerebral  Localization:  Ganglia  at  Base 


TABLE  Or 

SYMPTOMS  D 

"  TRANSVERSE  LESIONS  OF  BRAIN  STEM  AND  CEREBELLUM 

Actions 

Secretory 

Paralysis  of 

Paralysis  of 

Lost  or 

Reflexes 

Ver- 

Muscle 

and  Other 

Seat  of 

Lesion 

Motion 

Sensation 

Impaired 

Altered 

tigo 

Ataxia 

Sense 

Disturbances 

Some,  or  all,  of 

None. 

Movement  Tendon 

Usually 

None. 

Normal 

Tremor 

the  ocular  mus- 

of eye- 

reflexes 

absent. 

resembling 

cles  (except 

ball.    Use 

increased, 

that  of 

external  rectus) 

of  contra- 

with 

paralysis 

on  the  same 

lateral 

Babinski 

agitans 

'Lesion 

side,  combined 

half  of  the  and  ankle- 

(Benedikt  s 

confined 

with  a  contra- 

body. 

clonus,  on 

syndrome). 

to  the 

lateral  hemiple- 

opposite 

(441) 

pes  or 
foot. 

gia,  usually 

side. 

complete. 

Cutaneous 

Hemiplegia 

reflexes 

1270 

alternans 

may  or 

Crura 

oculomotoria. 

may  not 

Cerebri 

(Weber's  syn- 
drome, 440). 

Contralateral 
hemianesthesia, 
or  hemianalge- 

be  in- 
creased. 

A  slow, 
rhythmic 

Lesion 

One  or  more 

sia  and  thermic 

Movement  Tendon 

Present. 

Cere- 

Im- 

tremor of 

confined 

ocular  muscles, 

hemianesthesia, 

of  eyeball. 

reflexes 

bellar 

paired. 

arm  and  leg 

to  the 

except  the 

or  both.    Deaf- 

normal. 

type. 

of  opposite 

tegmen- 

abducens. 

ness  may  be 

side  may  be 

tum. 

present,  if  lesion 
be  bilateral. 

present . 

'Lesion 

Bilateral,  more 

May  be  blind- 

Movement 

Pupil 
reflex  lost 

Usually 

May  be 

Normal 

Nystagmus  (at 

confined 

or  less  exten- 

ness without 

of 

absent. 

absent. 

times  vertical), 

to 

sive,  of  all  ocu- 

choked disc  or 

eyeball. 

to  both 

squint ,     pupils 

anterior 

lar  muscles, 

other  lesion. 

light  and 

often  unequal. 

pair 

except  the 

accommo- 

1271 
Corpora 

(nates). 

abducens. 

dation. 

May  be  slow. 

Quadri- 

Lesion 

None  or  may 

May  lie  deaf- 

None, 

Normal. 

Usually 

Present . 

Normal 

rhythmic 

gemina. 

confined 

be  slight 

ness,  if  lesion 

except 

present. 

Of  cere- 

tremor of  arm 

to 

paralysis 

be  bilateral. 

chewing 

bellar 

and  leu  of 

posterior 

as  above,  or  of 

at  times. 

type. 

opposite  side, 

pair 

trochlearis. 

as] tally  on 

^(testes). 

voluntary 
motion. 

1272 

None. 

None. 

Walking 

Normal 

Usually 

Cere- 

Normal 

Nystagmus 

Cere- 

and 

or 

present. 

bellar 

(80),  tendency 

bellum. 

standing. 

slightly 

exagge- 
rated. 

ataxia 
with 

to  fall  to  one 

side,  occipital 

hypo- 

headache it 

Rarely 

tonia 

frequent . 

abolished 

almost 
always 

■  Hai- 
ti!.s  may 

1273 

None. 

None. 

\\*;i  Ikiri^r, 

Normal 

Usually 

Usually 

Normal 

Tendency  to 

Middle 

standing 

or 

present 

fall   or  to  turn 

cere- 

ami 

■lightly 

with 

Bad  or 

bellar 

sit  tins. 

exagge- 

hypo- 

bo.ly to  one 

peduncles. 

tonia 

side.    1; 

i>f  tin' 

movements, 

more  oi 

bellai 

pronounced) 

type 

choreii 

in  homolateral 

of  inforifir  ccrebcl 

ar  pedunelei 

■ion ;  those 

half  of  body. 

»f  the 

superior  cerebelku    peduncli                  -   neiform  move- 

ami  vertical 

menta  and 

divergence  of 

tin-  eyeballs 

imes 

occur, 

1274  Fracturt  he  above  syn  ling  to  their  po 

but  their  early  and  paralysis  ol  aptoms 

Cranium  of  paralysis  predominate  irritation. 

Involve  1 1 ntire  lateral  half  of  tin'  In  •  it  any  point 

I  in-   ymptoms  of  tbi  lepend  upon  the  f tlon  (physiology)  ol  the  pari  affected  and  will  natur 

ally  \  rhe  location  "i  ruch   ■  lesion  in  a  ti  ,;  «  "ill  depend  upon  what  longitu- 

dinal Boer  tracts  an  Involved,  and  In  longitudinal  Notion  upon  what  cranial  nuclei  and  nt 
Involved,  as  shown  bv  the  symptom    present  in  the  end  of  this  book 

■ntfa]  for  the  localisation  of  sue!  l  »iii  serve  'in-  purpose 

description 

221 


CHART  XXI  c 

Cerebral  Localization:  Ganglia  at  Base 

LOCALIZING  SYMPTOMS  IN  LESIONS  OF  GANGLIA  AT  BASE  OF  BRAIN 


Seat  of  Lesion 
1275 

Optic  Thalamus. 
(Fig.  17) 


'  Nucleus 
Lentic- 
ularis 
and 

Nucleus 
Cauda- 
tus. 


1276 
Corpus 

Stri- 
atum. 
(Fig.  17) 


Inter- 
nal 
Cap- 
sule. 


1277 

Corpus  Callosum. 

1278 

bland  of  Kiel. 
Claustrum  and 
External  capsule. 
(Fig.  17) 

L279 

1'ituitarv  Gland. 


1280 

Pineal  Gland. 


Diagnostic  Symptoms 
Symptoms  are  variable  and  uncertain.  May  be  hemianopia  (pulvinar,  and 
external  geniculate  involvement)  with  hemiopic  pupillary  reaction,  contra- 
lateral hemianalgesia.  Rigidity,  choreiform  movements,  athetosis,  and 
incoordination  of  contralateral  leg,  arm,  and  half  of  face  may  be  present. 
The  above  mentioned  motor  disturbances  occur  also  in  lesions  just  external 
to  the  optic  thalamus  which  involve  the  fibers  connecting  the  thalamus  with 
the  cerebral  cortex.  Sensory  disturbances  (pain,  hemianesthesia  dolorosa, 
anesthesia,  loss  of  muscle  sense)  may  be  present  in  the  same  parts.  Occa- 
sionally a  slight  irritation  of  the  skin  is  not  felt  at  all,  while  a  stronger 
one  is  felt  inordinately.  Absence  of  emotional  expression  in  face,  even 
when  not  paralyzed.  Vaso-motor  disturbances  may  occur  in  opposite 
side  of  body.  Isolated  analgesia  or  thermic  anesthesia  does  not  occur 
in  lesions  above  the  optic  thalamus,  but  other  forms  of  anesthesia  do. 

No  diagnostic  symptom  except  the  hemiplegia  due  to  the  involvement  of  the 
internal  capsule.  In  rare  cases  a  lesion  of  the  nucleus  lenticularis  may  be 
of  such  a  form  as  to  injure  the  anterior  and  posterior  part  of  the  posterior 
limb  of  the  internal  capsule,  while  its  middle  part  escapes.  In  such  cases 
there  results  a  hemiplegia  which  involves  the  leg  and  face  more  than  the 
arm.  Dysarthria  is  a  not  uncommon  symptom  and  in  some  cases  the  symp- 
toms of  sensory  irritation:  muscle  spasm  and  incoordination  described  under 
lesions  of  the  optic  thalamus  have  been  present.  When  the  ganglia  on  both 
sides  are  affected,  voluntary  voiding  of  urine  may  be  impossible,  while  auto- 
matic involuntary  voiding  may  occur  at  regular  intervals. 

Lesions  in  the  anterior  limb  of  the  internal  capsule  cause  either  no  symptoms 
or  a  paralysis  of  contralateral  half  of  face.  There  may  be  ataxia  and  athetoid 
movements. 

Lesions  in  the  anterior  two-thirds  of  the  posterior  limb  of  the  internal  capsule 
cause  a  total  contralateral  hemiplegia  of  the  body.  This  hemiplegia  con- 
sists purely  of  a  muscular  paralysis  and  never  produces  a  paralysis  of  the 
cortical  functions  such  as  aphasia,  alexia,  etc;  but  may  produce  dysarthria. 

Lesions  in  the  posterior  third  of  the  posterior  limb  of  the  internal  capsule 
cause  hemianesthesia  and  loss  of  muscle  sense  on  the  opposite  side  of  the 
body. 

Lesions  at  the  extreme  posterior  end  of  the  posterior  limb  of  the  internal 
capsule,  in  addition  to  hemianesthesia,  cause  contralateral   hemianopia, 

deafness  only  if  the  lesion  be  bilateral  and  often  the  symptoms  of  motor 
irritation,  described   under  lesions  of  optic  thalamus. 

No  diagnostic  symptoms. 

Lesions  in  this  area  produce  disturbances  of  speech,  grouped  under  the  general 
term  paraphasia,  and  may  produce  anarthna,  the  result  of  complete  aphasia. 


Hypertrophy,  tumor,  hemorrhage  and  some  other  lesions  of  the  gland  asso- 
ciated with  excess  of  secret  ion  may  cause  acromegaly  Or  gigantism,  in  ad- 
dition  to   a    progressive  hi  temporal  hemianopia,  terminating  in  blindness. 

\  defect  or  atrophy  of  the  gland  associated   with  a   diminution  of  secretion  m 

early  life  [nay  cause  dwarfism  and  may  produce  pituitary  eunuchiamua  or 

adiposogenital  degeneration  with  excess  Of  fat  and  a  defect  in  the  formation 

of  the  genitals,  in  any  case  of  pituitary  disease  there  may  be  polyuria. 
polydipsis  and  occasionally  glycosuria  and  very  rarely  an  escape  of  cerebro- 
spinal fluid  from  the  nose  (hydrorrhoea  nasalis).     In  some  oases  of  pituitary 

disease   there  are  no  symptoms. 

Abnormal  growth  of  hair  and  deposition  of  fat.    Abnormalities  of  genitals  tat 

times    with    attacks    of   seMlal    e\cit  etuent  I   xcessive    growth    in  height   of 

body  (dyspinelismus).  In  consequence  of  involvement  of  adjacent  tissue. 
bilateral  ocular  paralysis,  nystagmus,  pupil  abnormalities,  ataxia,  and  |wr- 
haps  disturbance*  of  hearing  may  be  present. 


CHART  XXI  d 

Cerebral  Localization:  Lobes  of  Brain 

LOCALIZING  SYMPTOMS  IN  LESIONS  OF  CEREBRAL  HEMISPHERES 


Seat  of  Lesiox 

1282 

FROxNTAL  LOBE 
Contains  the  centers 
for  all  the  skilled 
acts,  especially  the 
left  lobe.    Large 
lesions  in  the  frontal 
lobes  may  cause  a 
change  in  character 
and  disposition  of 
the  patient.    Many 
lesions,  especially 
tumors,  cause  Jack- 
sonian  epilepsy, 
especially  when  sit- 
uated in  posterior 
part  of  lobe;  while 
lesions  in  anterior 
part  of  lobe  may 
cause  epileptiform 
convulsions.     Ataxia 
sometimes  occurs  in 
tumors  in  the  fron- 
tal lobe.     (Fig.  15) 


1283 

PARIETAL  LOBE 
Contains  the  centers 
for  cutaneous  and 
muscular  sensation. 
Many  lesions,  espe- 
cially tumor,  cause 
Jacksonian  epilepsy 
when  situated  in  the 
anterior  portion  of 

this  lobe;  while 

berior 
portion  may  cause 
epileptiform  con- 
vulsion.-.    (Fig.  15) 


Diagnostic  Symptoms 
'Lesion  in  the  upper  fourth  of  this  convolution  may  cause 
Jacksonian  epilepsy  commencing  in,  and  motor  paralysis 
of,  the  contralateral  leg.  Very  large  lesions  (hemorrhage, 
tumors,  etc.)  in  this  region  may  cause  also  paralysis  of  the 
homolateral  leg  in  a  lesser  degree. 

Lesions  in  the  middle  half  of  the  convolution  may  cause 
Jacksonian  epilepsy  commencing  in,  and  awkwardness  of  or 
loss  of  skill  or  complete  paralysis  of,  the  contralateral  arm. 
Very  minute  lesions  in  the  upper  part  of  this  region  may 
affect  only  the  shoulder;  in  the  lower  part,  only  the  hand. 

Lesions  in  the  lower  fourth  of  this  convolution  may  cause 
Jacksonian  epilepsy  commencing  in,  and  paralysis  of,  the 
contralateral  half  of  face  and  neck.  Very  minute  lesions  in 
the  upper  part  of  this  region,  may  affect  only  the  eyes;  in 
the  lower  and  anterior  part,  the  tongue  and  larynx. 


The 

ascending 
frontal 
convo- 
lution. 

Lesions 
in  this 
region 
may 
cause 
awkward- 
ness 

(cortical 
ataxia, 
apraxia) 
rather 
than 
paralysis. 

The  base  of  the  Small  lesions  in  this  area  may  cause  in  right-handed  per- 
middle  left  fron-  sons,  argaphia,  and  in  many  cases  Jacksonian  epilepsy, 
tal  convolution.       commencing  in  the  contralateral  arm. 

The  base  of  the  Small  lesions  in  this  area  may  cause,  in  right-handed  per- 
inferior  left  fron-  sons,  motor  aphasia,  and  in  many  cases  Jacksonian 
tal  convolution.       epilepsy,  commencing  in  the  right  side  of  the  face. 

'Lesions  in  the  upper  fourth  of  this  convolution  may  cause 
some  blunting  of  cutaneous  sensibility,  and  especially 
astereognosis  in  contralateral  leg  and  foot. 


The 

ascending 
parietal 
convo- 
lution. 


1284 

TEMPORAL  LOBE 

•  lontains,  on  the  left  side,  tin-  o< 

of    Bensory     speech.         Lesions     may 

cause  epileptiform  convulsions. 


Lesions  in  the  middle  half  of  this  convolution  may  cause 
some  blunting  of  cutaneous  sensibility,  and  especially 
astereognosis  in  contralateral  arm  and  hand. 

Lesions  in  the  lower  fourth  of  this  convolution   may  cause 
some    blunting    of    cutaneous    sensibility,    and    especially 
bereognoeis  in  contralateral  half  of  face. 

The  left  ang-     Deep  lesions  in  this  region,  in  right-handed  persons  may 

ular  gyrus.  cause  alexia  and  hemianopia. 

The  reel  of  t  lie     Lesions  in  this  region  may  cause  loss  of  muscular  sense  and 
parietal  cortex,      motor  ataxia  in  the  contralateral  arm  and  leg. 


i  esione  in  the  posterior  portion  of  the  left  superior  tem- 
poral convolution  in  right-handed  persons, may  cause  sen- 
Bory aphasia  (psychic deafness). 


1286 

OOCIPITA]    LOBE 
( Sontaine  i  he  centers 
of  Bight .    Lesions 
may  cause  epilepti- 
form eonvul 
(Fig 


Neigh- 
borhood 
of 
oaloarine 


occipital 

.  lobe. 


■    in    this    area    cause   contralateral    homonymous    hemi- 
anopia.    A  lesion  limited  i"  'lie  superior  lip  <'t"  this  i 

iiadrantio  hemianopia  or  tetartanopia  of  the  con- 
tralateral lower  quadrants  of  field  of  vision.  A  lesion  lim- 
ited to  the  inferior  lip  of  this  fissure  causes  lOBB  of  contra- 
lateral upper  quadrants  of  the  field  of  vision. 

Lesions  in   this  area  may  cause  loss  of  power  of  recognition  OJ 
OS  and  things  (psychic  blind:. 


1286  Man\  lesions  cause  ■  mixture  of  paralysis  and  convulsions  over  ■*  limited  area 

Cortical  Lesions.  which  in  some  cases  maj  slowly  grov  larger.    The  intelligence  of  the  patient 

(Fig.  15)  is  always  more  or  lest  impaired. 


CHART  XXII 

Cerebro-Spinal  Localization 


TOPICAL  DIAGNOSIS 

LOCALIZATION  OF  LESIONS  FROM  ANALYSIS  OF  SYMPTOMS 

T1294 


1292 

The  reflexes  in  the  para- 
lysed area  are  abolished 
(except  in  1310  and  1329)  < 
A  lesion  of  the  peripheral 
neurons. 


1290 
PARALYSIS 

The  most  important 
of  all  localizing 
symptoms. 


Sensation  alone,  in  all  its 
forms  is  lost  or  impaired. 


1295 

Motion  alone 

impaired. 


is   lost   or 


1296 

Both  motion  and  sensa- 
tion are  lost  or  impaired.  „ 


•See  Chart   XXII  a. 


1297 

Special    forms    of 

pheral  paralyses. 


pen- 


1293 

The  reflexes  are  present 

(except  in  1357  and  1359)  - 

A  lesion  of  the  central 

neurons. 


1298 

Sensory  paralysis  domi- 
nant. Little  or  no  motor 
paralysis. 

1299 

Motor  paralysis  domi- 
nant.    Little  or  no  sen- 
sory paralysis. 

1300 

Both  motor  and  sensory 
.  paralysis  well  marked. 


See  Chart    XXII   b. 


See   Chart    XX 11   c. 


See  Chart   XXII  d. 


Bee  Chart    XXII  e. 


1291 

"iiian  Epilepsy,  together  with  other  symptoms  <>f  cerebral  disease. 

I  ox  diseases  and  lesions  accompanied  l>y  motor  paralyrit  see  469,  l>y  motor  spasm  see  570,  by 
ntiiriii  see  638,  by  tremor  see  889,  by  nystagmus  Bee  840,  by  fibriDaHon  Bee  841,  by  local  paralysis 
Bee  636,  by  local  spasm  sec  (i.'iT,  by  disorders  <»/  speech  sec  735,  by  disorders  <>/  gasi  see  73ti.  by 
anesthesia  and  anatgosia  see  810-12,  by  disorder*  of  special  senses  see  807-9,  by  paw  see  881,  by 
vertigo  see  982,  by  menial  disorders  gee  1038,  by  (ropnie  disorders  see  1120,  by  raso-motor  disorders 
•  •    1129,  by  ganglionic  disorders  Bet    1128,  by  syphuie  Bee  120">.  l>v  abnormal  eerebro-epinal  ,'/ui</ 

BO    1220. 


227 


CHART  XXII  a 

Cerebro-Spinal  Localization   Paralysis  with    Abolished 

Reflexes 


TOPICAL  DIAGNOSIS 
LOCALIZATION  OF  LESION  FROM  ANALYSIS  OF  SYMPTOMS 
Diagnostic  Symptoms  and  Tests 


'Area  of  anesthesia 

Onset 

1294 

etc.  lies  within 

acute 

Sensa- 

the area  of  distri- 

or sub- 

tion 
alone, 

bution  of  one  or 
more  nerves. 

acute. 

in  all 

its 

forms, 

Area  of  anesthesia 

Onset 

is  lost 

etc.  lies  within 

acute 

or  im- 

the area  of  distri- 

or 

paired. 

bution  of  one  or 
more  nerve  roots. 

chronic. 

The  paralysis  is 

Onset 

limited  to  muscles 

acute  or 

1295 

supplied  by  one 

6ub-acute 

Motion 

or  more  nerves. 

No  fever 

alone 

(Figs.  19-21 ) 

at  onset. 

is  lost    , 

or  im- 

paired. 

The  paralysis  is 

Onset 

limited  to  muscles 

acute  or 

supplied  by  one 

chronic. 

or  more  nerve 

May  be 

.roots.  (Figs.  19-21)  fever  at 

onset. 

Localization 
Lesion  is  in  one  or  more  sen-  1301 
sory  cranial  nerves  or  nuclei  or 
sensory  end-organ;  the  nerve 
affected  depending  upon  its 
anatomical  distribution  (822). 
(Figs.  19-21,  33,  38). 

Lesion  is  in  corresponding  sen-  1302 
sory  nucleus  in  the  brain  stem, 
or  in  the  posterior  horn  of  spinal 
cord,  or  in  column  of  Burdach, 
or  in  posterior  nerve  root. 
(Figs.  19-21,  24-6). 

Nerve  involved,  if  palpable,  is     Lesion  is  in  one  or  more  motor  1303 


Nerve  involved,  if  palpable,  is 
tender  on  pressure.  No  symp- 
tom of  disease  of  central  organs 
usually,  unless  nuclei  are  af- 
fected. 


Nerves  involved,  if  palpable, 
are  not  tender.  May  be  symp- 
toms   of    disease    of    central 


tender  on  pressure.  No  symp- 
toms of  disease  of  central 
organs.  All  the  muscles  sup- 
plied by  the  nerve  are  para- 
lysed, usually. 


cranial  nerves,  or  a  mild  lesion 
of  mixed  spinal  nerves;  the 
nerve  affected  is  the  nerve  sup- 
prying  the  paralysed  muscles 
(489-93).    (Figs.  19-21,  33,  38). 


1296 
Both 
motion 
and 

lion 

are 

loaf 

or  mi 

poind 


Motor  and  sensory 
paralysis  is  within  the 
area  of  distribution  of 
one  spinal  nerve. 

Motor  o  r  sensory 
paralysis  is  within  the 
area  of  distribution  of 
several  nerves  from 
one  plexus. 


Nerve  involved,  if  palpable,  not  Lesion     is     in     corresponding  1304 

tender.     May  be  symptoms  of  motor    nucleus    within    brain 

disease  of  central  organs.  Often  stem,   or  in   anterior  horn  of 

only  a  portion  of  the  muscles  spinal  cord,  or  in  the  anterior 

innervated  by  the  nucleus  are  nerve  root  (493-5).  Figs.19-21, 

paralysed.  24-6). 

'Lesion    in    one    spinal    nerve  1305 
(489).     (Figs.  33,  38). 


Onset 
acute 

or  sub-     Nerve  involved ;  tender, 
acute.      on  pressure.   No  symp- 
*  No  toms  of  disease  of  cen- 

fevrr         tnil  organs, 
at 

onset. 


Lesion  in   brachial   or  lumbar  1306 
plexus  (490).      (Fig.  32,  38). 


Motor 

and 

sensory 

paralysis 

extends 

Over 

legs  or 
arms  or 
both, 
or  even 
more 

,  illy 


Onset 
unite 

or  sub- 
acute 

May 

rarer 

Ml 
OlIM't 


'Nervee  involved  tender  Muscles  show  weak-  Lesion  of  many  spina]  1307 

on  pressure.  Nosvmp-  aeas,  tenderness  and  and    (rarely)    cranial 

toms  of  disease  of  con-  rapid  atrophy.  nerves  also   (multiple 

inil  org  neuritis)  HS8). 

Qreatpain.  May  be  deformity  Lesion  of    1808 

Lag)  .done     of  lumbar  spines    Symptoms  oauda 

are  para-        less    symmetrical    and    bed-  equina 

lyaed  and       sores   less  common   than    in  187 

involved        exhibit  lumbar  lesions.     Domain  of  (Fig   - 

not  tender.      trophic  anterior  crural  nerve  may  be 

There  are       disturb-  ,  normal  when  lesion  is  low, 
disturb-          at 

leaia      Little  pain.    May  be  de      Lesion  of  lum-   1309 
organic        'of  rectum       fortuity  of  lower  dona]    bar  enlargement 
reflexes  and  spinas    Symptoms  lym-    of  spin  J  cord 

and  other      bladder  metrical      ivd-sores  al-    (484  7) 

symptoms  ways    present         tfa 

Of  Organic  lion  of  legs  csca|H\ 

central  Both     Icirs    and     arms    an-    paralyzed        Lesion  of  OSr-       1310 

ire  trophic  dist  urbanees  in  ami    vioal  enlargement 
liu    do(  in  legs    Reflexes  are  abolished    ol  ipinal  oord 
.in  army,  exaggerated  in  legi    548-81)     (Fi| 


2  19 


CHART  XXII  b 
Cerebro-Spinal  Localization 

'  'ompritring  Numbers  1297  and  1315  to  131*7  on  left  side  of  charl 
:md  ms  to  1336  <>n  righl  margin 


TOPICAL.  I 
LOCALIZATION  OF  LESION  FF 


,  1315 

I  DISTURBANCES     OF 
VISION.     (807.) 


1297 

SPECIAL   FORMS    OF 
PERIPHERAL       PAR- 
ALYSIS.     REFLEXES   < 
\l'.'  ILISHED  IN   PAR- 
ALYSED AREA,  EX- 
<  KPT  IN  1329. 


1316 

PARALYSIS  OF  OCU-   < 

LAR  MUSCLES  (700). 


1317 

FACIAL  PARAL- 

'•YSIS  (703). 


PERIPHERAL  PARALYSIS  W  I 

DIAGNOSTIC  SY.M   (. 

'Blindness  of  entire  field  of  vision  of  one  eye  is  present     n 
light. 

Bitemporal  hemianopia  is  present.    The  outer  baU  of  eai  9 

is  present. 

Nasal  hemianopia  is  present.     The  inner  half  of  field  of 
is  present. 

Homonymous  hemianopia  is  present.    Identical  halves  (r  I 
pupillary  reflex  is  present  i.e.  reflex  is  absent  when  para 

'All  muscles  of  one  eye  paralysed.     Eyeball  protruded  or   I 

rNo  hemiplegia.     Other  crani 

All    muscles    supplied    by     i 

third    cranial    nerve    are  J  Paralysis  of  arm  and  lee  of  oi 
paralysed  at  once. 

Tremor  of  arm  and  leg  ol  op 
I    causing  ataxia. 

Partial  or  progressive  paralysis  of  muscles  supplied  by  thir 
No  hemiplegia.     Other   crani 


J  Paralysis  of  external  rec- 
tus muscle.  1  Hemiplegia  often  combine,. 
of  conjugate  deviation   of 
I     be  involved. 

Lower    branch    of    facial      Other  symptoms  of    : 

only,  or  mainly,  paralysed.  tion  never  present        Reflex 

'Paralysis  of  arm  and  lei:  of  oj 

No  hemiplegia.     Chronic  col 
and  abducens,  ma 

Associated  with  unilateral  di 


Both  lower  and  upper 
brandies  of  facial  nerve 
equally  paralysed. 


No  deafness  but  hyperakusis 
notes,  and  often  the  high  i 
times  absence  of  secretion 

Hyperakusis.      Loss  of  tasti    il 


No  hyperakusis.      Loss  of  Last 
No  hyperakusis.     No  loss  of  t 


GNOSIS 

1  ANALYSIS  OF  SYMPTOMS 

H  ABOLISHED  REFLEXES 

ItSANDTESTS  LOCALIZATION 

tic    n.-rve  is  atrophied.     Pupil  does  not  respond  to       Lesion  in  optic  nerve  (887-8).  I  ;is 

id  of  vision   is   blind.     Bemiopic   pupillary  reflex      Lesion  is  in  the  central  part  of  ootie  chiasm    362      L3tfl 

815.  860,  892 

on  of  one  eye  is  blind.     Hemiopic  pupillary  reflex      Lesion  is  in  outer  margin  of  optic  chiasm   (362,     1320 

815,  861 

or  left)  of  each  field  of  vision  is  blind.     Hemiopic      Lesion  is  in  the  optic  tract  or  external  geniculate     1321 
I  "J!  ol  retma  is  excited  by  light.  body  of  opposite  side   858 

cr  evidence  of  disease  within  orbit.  Lesion  within  theorbil    91  1  1322 

lerves  paralysed.  Leaion  of  3rd  cranial  nerve  trunk  or  nueleua  (700)      1323 

Fig    is 

Lesion  involving  crus  cerebri  (676  1324 

present  at  rest  and  exaggerated  on  motion,       Lesion  of  red  nucleus  or  rubro-epinal  tract  on  >.• 1325 

side  as  motor  oculi  parol;  1 

'""'■'''  ""rv"  '7I,°  Lesion  of  3rd  crania)  nucleus,  in  wl ■  or  in  part     1326 

(700)      (Fig    is 

fcrves  paralysed,  especially  the  facial.  1.   ion  of  6th  cranial  nerve  or  nuoleus     1330-1)      1327 

(Figs    19,  -'11  ) 

hemianesthesia  of  opposite  side.     Loss  of  power      Diffuse  lesion  of  Pons   Varolii   (539,883)      fFias      1328 
ight  or  left      Facial  or  auditory  nerve  may  19,20.) 

•  brain  present.     Electrical  reaction  of  degenera-      Lesion  above  nucleus  of  facial  nerve  in  cerebral  1329 

hemispheres  or  in  crura  cerebri.     (Fig    15 

lands     Often  abducens  par  Lesion  in  Pons  Varolii       Figs    19,20.)  1330 

Omially     Other  cranial  nerves,  especially  auditorj       Leaion  of  nucleus  of  facial  nerve       Figi    19,20  L381 

land  vertigo  without  disease  oft] u  Leaion  of  facial  nerve  trunk  at  base  of  brain  (Fig 

""." auriurn,  due  to  stapedius  parol    i       Lou       Leaion  of  nerve  above  geniculate  ganglion  (9281      1833 

ire  painful  to  bear.     No  lo  tl  1  1  gmgnon   u_m.     i.u.i 


|N«two-»Wi  l  1. acial  nerve  between  geniculate  ganglion 

and  stapedius  branch     1 1  ■■    IQ 

nnt-rmr  two-thirds  of  tongue  of  an  1 1  facial  nerve  between  stapedius  and  1 

tymp  i  ,      :,, 

I    Tenderneaa  near  stylo  mastoid  foramen  1  ,   ,,,,,,,1  facial  nerve  below  chorda  tympani  bi  inch      1  I3fl 

(Fig 


CHART  XXII  c 
Cerebro-Spinal  Localization 

I  Comprising  Numbers  1298  and  L340  to  1346  <>n  Kit  side  of  Charl 
and  1347  to  iHti'.i  on  ri^lit  margin. 


L340 

ANESTHESIA      with 

without   ANALGESIA. 


DIAGNOSTIC  SYMPTOMS  AND  TESTS 

Marked  ataxia. 
Limited  to  one  or  both  legs 

[Slight  ataxia. 
Limited  to  one  arm.  Slighl  ataxia 

In  both  anus  and  both  legs.      Marked  ataxia 
Marked  ataxia. 


In  arm  and   leg  of  SO 


mi'  side. 


Slighl  ataxia. 


TOPIC/ 
LOCALIZATION  OF  LESION 
ANESTHESIA  WITH 


Anesthesia  marked,  bilateral. 
of  muscle  sense, 

Anesthesia  slighl  and  most  mt 
be  cerebral  symptoms,  Jacks* 

Anesthesia  slight,   most    marked 

cerebral  symptoms  (Jackson  i 

May    lie    other   spinal    symptom 
in  arms  and  legs, 

May  la-  other  spinal  symptom 
in  arm  and  leg. 

Anesthesia  sli«;ht.  moat  marked  i 
he  other  cerebral  symptoms, 


irs&lfjsr  «* +■   >%%%s«- — 


I  In  arm.  leg  and  face  of  same        Slighl  ataxia 

side. 


1298 

s  i:\sojn 

PARAL1  SIS 
DOMINANT. 
LITTLE  OR  NO 
MOTOB    PARAL- 
VS1S.     TENDON 
REFLEXES  PRE- 
SENT OR 
EXAGGERATED. 


L341 

ANALGESIA  unh  THER- 
MIC ANESTHESIA,  l>.n 
litl  li  oi  no  tactile  anesthesia, 
is  present.  DISSOCJ  ATION 
id   SI  NSATION. 


In     oi r     both 

legs. 


Usually  unilateral. 


Usually  bilateral. 


I  No  Jacksonian  epilepsy      Hernia 

Jacksonian  epilepsy  common. 
No  trophic  disturbances.     \i 


Trophic  disturbances   in   legs. 
usually  abolished,  especially 


(Tsnally   unilateral.      Leg  of     No  trophic  disturbances     Ofti 

nn  mi  >   on  i<    a  L, ,    in.',  J.  ...  I 


In     one    or     both     , s:'""'  sil1''  als"  involved 


In  arms,  or  legs,  or 
both, 


I'sualh    bilateral.      Legs   of     Tropin,-   disturbances   in   arms 
-normal  sensibility.  especially  in  advanced 

[Bilateral  usually,   marked  May  I ther  spinal  symptom. 

ataxia.  plegia). 

f  Eiemianopia  and  anesthesia  ii  in 

J  Jacksonian  epilepsy  and  other  e< 
]     present 


1342 
HOMONYMOUS 

1IKMI  Wtil'l  \ 

1343 

HOMON1  Mors 
TETARTANOPIA,  QUAD- 
RANT HEM!  ANOP1  \ 

1344 

P8YCHIC  HI. I. \ dm  SS 

"l:>    APHASIA, 

1346 

AS!  I  REOGNOSI8. 


H'nilateral,  slight  ataxia. 

Jn  contralateral  arm  and  leg  with 

''''■""'^  ll:ilv"s  *'r  '■"■>'  field  of  visi righl  or  left)  are  blind.     No  hemiopic  pupillarj  i 

M"'l,";:l'1  quadrants  of  each  held  of  vision  (right  or  left)  are  blind.     No  hemiopic  pur, 
anesthesia  or  other  paralysis.     May  be  other  cerebral  symptoms. 

Patienl  is  not  bhnd,  bul  cannot  recognize  things  by  sight,  though  he  may  by  touch  or  N 
Pme^or^nfOTsJp^k,en>UwoX0i  wdm>mA  worda  s,,"k""  '"  ll""'  ttlthou6«  '" 
Patient  is  not  anesthetic,  or  very  slightly  so,  bul  cannot  recognize  objects  by  the 


IAGNOSIS 

3M  ANALYSIS  OF  SYMPTOMS 

GGERATED  REFLEXES 

LOCALIZATION 

spinal  symptoms,  especi  -IK   loss      Lesion  in  one  or  both  posterior  columns  of  cord  in  dorsal  reg Same  ride  if  unilateral     1347 

34-6.) 

m  foot. _   Aim,,..,  always  unilateral.     May      Lea^r^in   upper^ne-fourth  of  posterior  central  convolution   in  contralateral  cerebral     1348 

fed,  astereognosis  marked.     May  be  other      Lesion  in  middle  one-half  of  posterior  central  convolution  in  contralateral  cerebral  cortex      I34i) 
Depsy).     Usually  some  motor  paralysis.  (Kg.  15  luuTuawsrai  cereorat  conex.     i.i.i 

ksarmoea  common.     Loss  of  muscle  sense      Lesion  of  posterior  columns  of  cord  in  cervical  region  (654a   785        Figs.  24^0  1350 

kpnoea  common.     U !  muscle  sense      Lesion  of  posterior  column  of  cord  on  same  aide,  in  cervical  region  (654a,  785       Pip  24-6.)     1361 

"' i',1" ', '"".'■     ^tereognoae  marked.     May      Leaion  in  i a  three-fourths  of  posterior  central  convolution  of  contralateral  cerebral     1352 

Bally  Jacksonian  epilepsy.  cortex.     (Fig.  15  ''    IJ '"•"     '•'-,- 

"'"       Pmly**  of  conjugate  deviation  of      Lesion  in   tegmenl , B    Varolii  on   same  ride   as   the   facial   anesthesia     883).     L353 

"'""""""'  l-'-|M"  of  posterioi    pari   of  internal  capsule  of  contralateral  hemisphere   (857,    1276).     1354 

hianopia.     Mental  deterioration.  Lesion  of  superior  parietal  lobule  of  contralateral  hemisphere    657).      Fig    15  i:;.v, 

Uee  of  organic  reflexes.     Usually  ataxia.      Lerion    in    peripherj    of   opposite    lateral    column    of   cord    in    dorsal    region      1360       1358 

24-6 

l,.:,"!1:  .;,,  |rcndon  reflexes  ***■  *  t^  r: ni iM"  :"""n"r unifure  -r ••' m  lumb« ™iw»™ -  tn  im 

central  gliosis  the  lesion  may  extend  upwards  to  the  cervical  enlargement  and  involve 
the  arms  secondaril]  (837-9,  1359  i 

f*  ""' '  '""  "'   rnu8cle  WMe'  l'1"-1""  '"  periphery  of  the  o] rite,  orol  both,  lateral unns  of  the  cord  in  theoervii  il     I  158 

regio  igf    S4-6.) 

"'""   ,'"11"''-   "-||:ilK    abolished    ii as,      Lerion  in  central  gray  matter  (anterior  commissure)  of  the  cord  in  cervical  enlanremenl     1358 

652,  693    837,-9   1009,   1170,   lis?.   1367)      (Figs.  2 

' ' »W»    spastic  para-      Lerion  of  lateral  columns  of  cord    664,1212,1366,1368,1396)       Figs.  2  1360 

Other  cerebral  symptoms.  Lesion  of  posterior  pari  ntralateral  internal  capsule    867        Fig    17.)  1361 

fa  symptoms  usually  present       Vneel is      Lesion  of  infer arietal  lobule  of  c alateri misphen     651         Fig    16.  1362 

1  •    on  ol  ponto    ■  rcbi  II  ir  angle  on  ride  of  deafness    138  i  ;,, . 

:'    0t»>w  oerebral  symptom.  I.,. irine  fissure  of  occipital  lobe,  o.  ol  fascioulus  of  Gratiolet  of  eon-     1364 

tteral  cerebral  hemisphere   362,815   890   1286        Fig    16 

Lower  quadrant  ol      Lesion  of  upper  lip  of  contralateral  1285        I  ,■■    n.  n,;-, 

'  i;i'"  •'""ll  ",l  ":      I ■'■  ""'  ol  lower  Iq sonti  ilateral  calci ■  fissure       I  i  i  ;,,,, 

field  of  visi 

L      "'    '•'  '  '""'  "*»'  ,"1"  I  occipital  lobeoflrfl  cerebral  hemisphej  ,  -.„; 

'""'  "'"  ""      "  I  oi   pari  ol   l.ii   rior  temporal  convolutioi 

15 

0U*hh8«nb     '  r«ght.      I.  ,nvo ,  ,. r:i|;lli    ,  ,  , 

phen 


CHART  XXII  d 
Cerebro-Spinal  Localization 

Comprising  Numbers  i-".*'.i  on  lef1  side  of  chart 
and  L372  to  L391  on  right  margin. 


235 


TOP  / 
LOCALIZATION  OF  LESI  ( 
MOTOR  PARALYSIS 


DIAGNOSTIC  SYMPTOMS  AND  TESTS 


I"/'";'1   to  one  or  fSymptoms  bilateral  usually.      May  be  other  spinal  symptoms 

'";  h  "*s-    Organic  *  of  sensation  rnlegs. 

reflexes  nol   dis- 

ordered.  LSymptoms  unilateral  usually.      May  be  other  cerebral  symptoms,  es] 

Limited     to     both  fNo  "insulv  paralysis.     No  cerebral  symptoms.    Often  ataxia  and 

arms  and  both  legs  J     :"'"ls  :""'  less 


L299 

MOTOB    PAR- 
ALYSIS  DOMIN- 
ANT     LITTLE 
ok  NO  SEN- 
SORY PARALY- 
SIS.   TENDON 
REFLEXES 
PRESENT  OH 
EXAGGERATED 


i  Irganic  reflexes  not    1  ,.      ,, 
disordered.  i  '  M1'    ■    """"'  -^''ison   paralysis.     Dysarthria  and  dysphagia.     Paral 

I     ing  with  position  of  lesion. 

Limited  to  one  arm.      Occasionally  some  slight  sensory  paralysis.    Jacksonian  epilepss   ai 
common. 

r Dissociation  of  sensation  and  ataxia  may  be  present.    Organic  n 
cerebral  symptoms. 

Limited  to  arm  and      ,  ■      ,, 

leg  of  same  side.       ^  Usually  some  sensory   symptoms.     Dysarthria    and   dysphagia    not 
|     crania]  nerves  frequent. 

U'sually  some  sensory  Symptoms,      .lacksonian  epilepsy  and  othi 


Limited  to  lower  branch  of  facial  nerve. 

Limited  to  arm  and  lower  branch  of  facial  nerve 


i    Jacksonian   epilepsy  and   other  syna 

common.     Often  complicated  with 


of  same  side. 

Limited  to  arm  and  leg  of  same  side  and  hypo-") 

glossus  nerve  of  opposite  side.  Usually  some  sensory  symptoms. 

..,.,  .  ,  r        Paralysis  of  some  other  crania 

Limited  to  arm  and  leg  ol   same  side  and   lower  abducens  paralysis 

branch  of  facial  nerve  of  opposite  side  J 

Limited    to   arm    and   leg   of  same   side   and    motor       Usually    some    sensory    symptoms 

ocuh  nerve  ol  opposite  side.  nerves  common 

("Usually  other  cerebral  symptoms  pn 
fSymptomsof  paralysis  rather    |     ,""1S' 

Limited  t<  i  arm  and        t  lian  of  irrit.it  ion       Not    pro-     1  ni. 

leg    and    lower  gressive.  Often  sensory  symptoms  present.     P 

branch  of  facial        <  '      pression  on  opposite  side  of 

nerve  on  same  side  .... 

.symptoms      ol       irritation        No  objective  sensory  symptoms,    ofi 

I  .lacksonian  epilepsy. 

m  SARTHRIA  Paralysis  of  some  of  the  cranial  nerves  and  usually  of  arm  and  lee  also 

and  DYSPHAG]  \ 


VOL'  M'JIIA  Loss  of  power  Of  Writing,  although  arm  is  nol   paralysed 

l.o.ss  oi  power  of    peaking  .some  or  all  words.     Limited  voi 

HlUSCleS  Ol    Speech  nol    paralyzed. 
Inability  to  read,  although  patient  can  see  and  can  speak 


MOTOB 

\l'll  \H  \ 

VLEXIA 


unary 


iL  DIAGNOSIS 

FROM  ANALYSIS  OF  SYMPTOMS 

rH  EXAGGERATED  REFLEXES 

LOCALIZATION 
itaxia  and  dissociation      Um^thgmOM^  a^tbath  lateral.  columns  „f  cord  in  dorsal  [372 

Oly  Jacksonian  epilepsy.      Leaon  of  upper  part  of  anterior  central  convolution  of  contralateral  hemisphere      137  ; 
cortical  or  sub-cortical  (leg  center).     fFig.  15.) 

ociation  of  sensation  in      Lesion  of  lateral  columns,  of  the  card  in  the  cervical  region  (626         1  igs   36-7       1374 

'"'  ""rv"~ v:i,v"  '"oi0:;;,,'^^)'  West-  "  ""-"■'  •?- h  *■ >**  »■>.,  m 

her  cerebral  symptoms      Lesion  in  cortex  or  QiddJ ,e*alf  of  anterior  central  convolution     i  176 

of  contralateral  hemisphere   arm  center]       Fig    15 

a  ■...!  disordered.     No      I  mtralateral  lateral  column  of  cord  in  cervical  region  (1131,  1141).     1377 

--  i-  I 

some      Lesion  in  the  brain  stem    in vohring  the  pyramidal  tract).     (Figs    19-22  1378 

ortical  disease.      Lesion  in  carta  or  sub-cortex  of  upper  three^ourths  of  anterioi  central  con-     1379 
rotation  of  contralateral  hemisphere.     (Fig    15.) 

rLeaon  in  cortex  or  sub-cortex  of  inferior  pari  of  anterior  central  convolution     1380 
U  of    cortical   disease    ,     0I  contralateral  hemisphere  (face  centei         Fig    1". 
«.r  apbi 

Lesion  o  cortex  or  sub-cortex  of  lower  three-fourths  of  anterior  central  oonvota-     1381 

(.    uon  or  contralateral  hemisphere  (arm  and  Fig    i.-, 

rtbria  and  dysphagia       '™  2]  """'""•''  ""  " ^  M  "'"  ***>&*«*  ***&*    rar odition).     1382 

•s  common,   especially 

Lesion  in  bridge  portion  of  pons  ....  same  side  as  the  racial  paralysis.     (Fig.  20       1383 

'   other  cranial      Lesion  ia  pee  cruris  cerebri  on  same  side  as  the  motor  oc aralysis.    (Fig.  19       1384 

aMOT3  « ■    l-'l;;;;:;,.'"  :";';;r^ ''""'  a  |"",",",r  l""1'  "f  n**™*  capsule  at  ,.,,,„,„.,■ 1„  „„,- 

." ' "  *  ,"Ci;:i,.,;;:,",r;,",r  rf  ■ »* a  -d *■  -* *.  «■ 

'""t"r   "'  Uaon  throughout  ai  ral  convolution  of  contralateral  hemisphere    oor-     1387 

lex  "i  sub-cortex        I  ig    i". 

Lesion  in  tegmentum  of  pons  or  i lulls    284-6        Figa   20-1.]  L388 

■  or  subcortical  lesion  al   base  of  middle  frontal  oonvolution  of  left     1389 
u  hemuphen   in  righl  banded  person    227,  77'.        I 

be  made  and      Corti.  „i  or  sub-,  urtical  fan ,  ,,,...  ,„■  „„,,„„  ,,.,,  ,„„lta|  ,,„„.„,„„„„  „,  ni;l„     , 

banded  i.-, 

*"l\     j  ""'  '""  «n«ulai rolution  in  righl  banded  p 


CHART   XXII  e 

Cerebro-Spinal  Localization 


1291 
J 
A 
C 
K 
S 
<) 
N 
I 
A 
N 

E 
P 

I 

L 
E 

p 

s 

X 


TOPICAL  DIAGNOSIS 

LOCALIZATION  OF  LESION  FROM  ANALYSIS  OF  SYMPTOMS 

MOTOR  AND  SENSORY  PARALYSIS  WITH  EXAGGERATED  REFLEXES 

JACKSONIAN  EPILEPSY 


r  Limited 

1300 

to  both 

Both 

legs. 

motor 

and 

sen- 

sory 

paraly- 

sis well 

marked. 

Reflexes 

Limited 

present 

to  both 

or  exag- 

arms 

gerated  , 

and  \ 

except 

both 

in  1396. 

.legs. 

Diagnostic  Symptoms  and  Tests 

'  Paralysis  severe.  No  ataxia.  Organic 
reflexes  much  disordered.  Some  of 
the  trunk  reflexes  are  lost.  Vertical 
extent  of  lesion  is  shown  by  the  ab- 
sence of  the  different  trunk  reflexes. 
Upper  limit  of  lesion  shown  by  the 
zone  of  hyperesthesia,  limiting  the 
anesthesia  above. 

Paralysis  not  so  extreme.  Marked 
ataxia.  Loss  of  muscle  sense.  Or- 
ganic reflexes  not  at  all,  or  slightly, 
disordered.  Trunk  reflexes  not  abol- 
ished. Knee-jerks  and  other  leg  re- 
-  flexes  may  be  increased  or  abolished. 

("No   involvement  of  cranial   nerves. 
Priapism.      Dyspnoea.      Very   dan- 
j  gerous,  usually  fatal. 


Involvement  of  some  cranial  nerves. 
Dysarthria    and    dysphagia.      Very 
'-dangerous,  usually  fatal. 


Spasmodic  twitching  of  head  and  eyes  to  one  side.  Twitch- 
ing may  remain  limited  to  these  muscles  or  may  extend 
to  other  muscles  of  face  and  neck  and  arm  and  later  to 
leg  of  same  side  or  may  finally  extend  to  muscles  of  both 
sides  of  body. 

Spasmodic  twitching  commences  in  one  side  of  face. 
Twitching  may  remain  limited  to  these  muscles  or  may 
extend  to  others  as  above. 


Spasmodic  twitching  in  hand  or  arm.  Twitching  may 
remain  limited  to  these  muscles  or  may  extend  to  face 
Or  to  leg  or  to  both  simultaneously  of  same  side  and  may 
later  extend  to  muscles  of  other  side  of  body  also. 

Spasmodic  twitohing  of  foot  or  leg.  Twitching  may  re- 
main limited  to  these  muscles,  or  may  extend  to  arm 

;ind  later  t<>  face  of  same  side  and  later  to  muscles  of 
other  side  of  body.     (Figs.  15,  16). 

Spasmodic  twitching,  commencing  simultaneously,  In  arm 
and  face  of  lame  Bide,  whioh  later  extends  to  muscles 

ill  the  \>x  of  the  same  side  and  still  later  to  muscles  of 

the  opposite  side  of  the  body. 
Spasmodic  twitohing  commencing  In  arm  and  leg  of  same 

side,  which   may  later  extend   to  face  Of  same  side  and 

may  later  extend  to  muscles  of  the  other  side  of  body. 


Localization 
Transverse  lesion  of  spinal  1395 
cord  in  dorsal  region. 
(Myelitis.)     (516-9,  829). 


Lesion  both  in  lateral  and  1396 
posterior  columns  of  cord. 
(Ataxic  Paraplegia.)   (526, 
660.  796)     (Figs.  25-7.) 


Transverse  lesion  of  spinal  1397 
cord  in  cervical  region. 
(512-5,  828)     (Figs.  25-6). 

Lesion   on   both  sides   of  1398 
brain  stem  (medulla,  pons 
or  crura   cerebri,   accord- 
ing to  cranial  nerves  in- 
volved).    (Figs.  19-21). 

Lesion  in  or  near  base  of  1399 
middle  frontal  convolution 
of  contralateral  hemisphere. 
(Fig.  15). 


Lesion   in    or   near   lower  1400 
quarter  of  the  central  con- 
volutions of  contralateral 
hemisphere.     (Fig.  15). 

Lesion  in  or  near  middle   1401 
half    of    the    central    con- 
volutions of  contralateral 
hemisphere.     (Fig.  15). 

Lesion  in  or  near  upper  1402 

quarter  Of  central  convo- 
lutions or  paracent  ral  lob- 
ule of  Opposite  hemisphere. 

Lesion    near    and    equally    140:? 
distant    from    motor    area 
of  face  and  arm  in  contra- 
lateral hemisphere.     ( Fin-  15)- 

Lesion   near  and   equally  1104 
distant    from   motor  ana 

Of  arm  and  lee;  in  emit  rs 

lateral  hemisphere.     ( Fie;  15), 


Spasmodic  twitohing  commencing  in  face  and  arm  and  lesion  in  inferior  parietal  l  i'1^ 

lee,   of   same   side,    which    may    later   extend     to    muscles  lobule    of    cunt  ralati  I]  al 

of  opposite  side,  hemisphere.     (Fig.  15). 

287 


PLATES 


Schematic  representation  of  the  convex  surface  of  the  left  cerebral    hemisphere,  showing  t lie  motor  and 
and  the  location  of  the  cortical  functions. 

See  1282-6,  1348  9,  1352,  L355,  1362,  1367  9,  1373,  1376,  L379,  1380   I.  1387,  1389  91,  1  loo  5. 


21(1 


Fio.   10 

Schematic  representation  of  the  medial  the  lefl  cerebral  hemisphere      U.  L.  Q.  Upper  left  quadrant 

of  retina      1.   I.  Q    Lower  left  quadrant  "i  retina 
Bee  852-3,  856,  1285,  1364-6,  1  102 


PACIAL  \       ARM         Lt 

HYPOGLOSSAL 


i  ra   17 

Horizontal  Section  thro         I  lemisphcre  showing  the  principal  I  psule; 

Kn.  Genu  oft  laic  Nucleus;  \l     Lenticulai   Nuclei!     ''I    Optic  I'hulnmuji 

Bp,  Splenium  ol  Corpi 


'II 


Nuil.  Comiss.  post.  et  | 
fasc   long,  dors,  i 

Fasc.  long  iters 

Klrfnzcll.  Oculom.-Kern 

M.  levator  palpebral: 

M.  obltquus  inferior 

M.  rectus  superior :.^.A.^. "'$  *^/ 

M.  rectus  inleriius 
M  jcctus  inferior 


Fig.  18 

Schematic  representation  of  the  nuclei  situated  beneath  the  floor  of  the  Sylvian  aqueduct,  showing  the  origin 

of  tlie  posterior  commissure, the  oculo-motor  ami  trochlearis  nerves,  as  well  as  the  nuclear  localizatii I  the  centers 

for  i  hi'  individual  ocular  muscles  (after  Edinger). 
s,r.  692,  Tim.  816,  1316. 


242 


I  n.  L9 

Schematic  representation  of  brain  stem;  showing  nuclei  and  nerve  roots. 
The  sensory  nuclei  and  nerve  roota  are  colored  red,  the  motor  blue. 
S«e  1301-1.  1323-32,  1353,  1375,  1378,  1398. 


248 


-  -Deiters  nucV 


pyramid 


Diagrammatic  transverse  section  through  the  pons  at  a  level  slightly  posterior  to  the  superficial  origin  ot  the 

trigeminus. 

See  1269,  1301-4,  1327-30,  1353,  1383,  1388,  1398. 


rued,  raphe 
i  post. long",  fasc. 


-N.sohtar. 


-  -V.  spinal  rt 

-  -subst.gelat. 
---N.arrVbig. 

«  dir.cerebel  tr. 
(Flechsig) 

- -ant  lateral  tr. 
(Gowers) 

x—  int. arcuate 
fibres 


Fig.  21 
Diagrammatic  transverse  section  through  the  medulla,  approximately  near  its  middle. 
See  1268,  1301-4,  1382,  1388,  1398. 

244 


coVG'oYl 

-Ti.  gracilis 
col.Burdach 
-n  cuneatus 

-  "Spinal  V 

— subst .  gel  at,. 
■  -mt.arcuatefr. 

—n 

— ant.Viorn 
— lemniscus 

olive 


Fio.  22 

TranEveree  section  of    medulla  just  above  motor  decussation  and  just  above  line    of    junction    with    the    cord, 
showing  the  sensory  decussation  and  the  topography  of  the  lowest  level  of  the  medulla. 

See  1268 


Fio.  23 

Transverse  section  of  the  cord  }uft  at  tin-  lirn-  of  junrtion  with  the  medulla,  showing  the  motor  decussation  and  the 
topography  of  the  uppermost  level  of  the  cord. 

Bh  L208 

24fi 


Fig.  24 


DIAGRAMMATIC  SECTION  OF  THE  SPINAL  CORD  TO  ILLUSTRATE 
ITS  PHYSIOLOGY 


Left  side  shows  situation  of  lesions  causing 
disorders  of  motion  and  sensation. 


Right  side  shows  situation  of  lesions  causing 
disorders  of  reflex  activity. 

Destructive  lesions  at  M  or  E  cause  diminution,  slight  irritative  lesions,  exaggeration,  of  motion.  Destructive 
lesions  at  S  cause  permanent  anaesthesia,  analgesia,  thermic  anesthesia  and  loss  of  muscle  sense.  Destructive 
lesions  at  T  cause  analgesia  and  thermic  anesthesia.  Destructive  lesions  at  P  cause  ataxia.  Destructive  lesions  at 
K  cause  loss  of  muscle  sense,  ataxia  and  anaesthesia.  Irritative  lesions  at  S,  K,  T,  or  P,  may  cause  exaggeration, 
or  perversion,  or  both,  of  sensation.  Destructive  lesions  at  D  cause  diminution,  and  at  E,  exaggeration,  of  reflex 
activity.     Slight  irritative  lesions  at  D  cause  exaggeration,  and  at  E  diminution,  of  reflex  activity. 

Symptoms  of  lesions  at  M  are  described  in  252,  263,  495,  547,  789;  1148-9,  1233  and  1304  at  E  in  251,  254, 
256,  525-6,  796-7  and  1212,  1372-4-7;  at  S  in  824;  at  T  in  1356-8-60;  at  P  in  281,  654;  at  K  in  280,  654a,  785, 
1302,  1347  and  1350-1,  1396.     The  results  of  lesions  at  D  and  E  are  discussed  in  Chart  V  a. 


Cervical  Enlargement 


Lumbar  Enlargement 


Fig.  25 


LOCALIZATION  OF  NUCLEI  IN  THE  ANTERIOR  HORNS  OF  THE  SPINAL  CORD 

(After  Edinger  modified  from  Sano.) 


246 


I  to.  26 


I  SCHEMATA    REPRE8EN1  VTION  OF   \  TRANS\  ERS1    SECTION  OF  THE  SPINAL  CORD;  SEVERAL 
LEA  ELS  BEING  COMBINED  IN  DO  ONI 


'       '.ITS 

\  S  i  -  vest  ibulo-epinal  1 1 

I  8  I  U pina]  trad 

1 1  I'  I  direct  pyramidal  I  spinal 

i  I',  i  .1  t  racl  *         trad 

■illllil 


\-i  i  NS1NG    lie  ICTBJ 

-  i    i  jpino-thalamic  i  rad 

V.S.C.1  interior  spino  eerebeU  Gowers  trad) 

P.S.C  l.  posterior Bpino-cerebellar trad    Flei 

('.('.  ( 'lark's  column 


On  the  left  side  of  the  cord  are  represented  the  nerve  roots  and  those  bundles  of  long  fibers  in  r  1 1 « -  white  col- 
umns which  carrj  impulses  downward  from  the  brain  i"  the  spinal  cord,  and  on  the  right  Bide  are  represented  those 

in  the  white  columns  which  carrj  impulses  upward  fi or  spinal  ganglia  i" 

n      li  hardly  needs  to  be  stated  that,  although  In  this  figure  these  long  bundles  of  fibers  are  repn 
mi  one  side  only,  the)  are  really  Bituatcd  Byniini  each  side  "i  the  cord.      Hie  short  fibers  wluch  conned 

different  levels  ol  the  cord  together  are  not  represented  in  the  figi 

us  involving  the  pyramidal  tract   Lim-  bed  under  251,  254 

1212  and  1372-4-7.     Les -  involving  tin-  anterior  horns  give  rise  to  atrophic  paralysis,  "I"  ol  which 

Bribed  under    196,  789,  1148,  1233    md    1304 ;  while  the  ol tie  formi  i lesoribed  under  .Mr.  895,   1149 

and  1304      Lesioru  involving  the  posterior  horn 

column  cribed  under  786,  1302,  1 3  17,  I860 

ribed    under  281  and  664.      Lesioi       f  the  spino-tha  of   the 

anterioi  ymptorus  described  under  305,  811  ami  i     6-00      I 

the  whole  of  one  lateral  half  of  thi  cribed  undor  142,609,  840  ind  981 ;  while  lesions 

of  the  whole  ti  cti i  the  cord  givi  ptomi  described  under  185,  513  I,  617  S 

md  980,  U48a,  i  109-10,  i 

247 


Fig.  27 
Schematic  representation  of  the  more  important  diseases  of  the  spinal  curd. 


See  345.  416,  U9  20,  133,  661,  756, 
784,  827,  891,  894,  911,  979,  987, 
Hint.  1015,  1172,  Use,  1217  and 
1231 


Locomotor  Ataxia 
(lumbar  region) 


Amyotrophic  Lateral  Sclerosis 


Acute  Stage    Chronic  Staff 
Anterior  Poliomyelitis 
See  116,  419,  495,  789  1 1 Is 
and  1233 


LoCOmotOl     \la\ia 

(cervical  region) 


See  547,  695,  707,  1149; 
and  525,  670  and  797 


Descending  Degeneration  of 
Pyramidal  Tracts 


Syringomyelia 

See  552,  693,  837-9,1009,  1150a 

1170,  1IS7,  1357  and  1359 


Mr,luii4  rmlcilli, 


Compression  Myelitis   with   the   conse- 
quent Ascending  and   Descending 
Degenerations.     See  520,  795. 

No.  3  shows  the  point  of  the  compression  with 
the  whole  transverse  section  of  the  cord  the 
Beat  of  an  inflamma 

No.   1    shows     ascending   degeneration    of    the 

columns  of  Goll,  of  the   spino-thalamte  tracts, 
and  of  the  anterior  and  posterior  spino-cerebellar 

I  raets. 

No.  2,  close  to  the  lesion,  shows  in  addition  a 
slight   degeneration  of  the  columns  of  Burdach. 

Nos.  4-6  show  degeneration  of  the  crossed 
and  direct  pyramidal  tracts  of  the  vestibulo- 
spinal, rubro-spinal,  and  I  halamo  spinal  tracts 
and  of  Schultze's  comma, 

The  upper  series  face  up  and  the  lower  down. 
248 


M.  .hill.    II. 


SCHEMATIC  REPRESENTATION  OF  SOME  POINTS  IN  THE  PHYSIOLOGY  AND  PATHOLOGY  OF 
THE  SPINAL  CORD  AND  PERIPHERAL  NERVES. 
Fig.  28.     Diagram  to  illustrate  the  mechanism  of  the  bladder  reflex 


B  represents  the  bladder.  S  C  rep- 
resents the  reflex  centre,  with  its  motor 
and  sensory  neurons,  for  the  sphincter  of 
the  bladder,  which  is  excited  to  action  by 
urine  in  the  neck  of  the  bladder  or  in  the 
prostatic  urethra.  DC  represents  there- 
flex  centre,  with  its  motor  and  sensory 
neurons,  for  the  detrusor  of  the  bladder, 
which  is  excited  to  action  by  the  disten- 
tion of  the  walls  of  the  bladder.  These 
two  reflexes  are  antagonistic  and  the  sen- 
sory surface  irritated  being  much  larger 
in  the  latter  (D  C),  than  in  the  former  (S 
C),  reflex,  the  detrusor  reflex  will  eventually 
overpower  the  sphincter  reflex  under  nor- 
mal conditions.  S  T  represents  the  sensory 
tract  connecting  the  bladder  with  the 
brain,  by  means  of  which  the  individual 
is  informed  as  to  the  degree  of  fulness  of 
the  bladder.  M  T  represents  the  motor 
tract  connecting  the  cerebral  with  the 
spinal  centre  by  means  of  which  the 
individual  can  inhibit  the  activity  of  either 
centre  (up  to  a  certain  degree)  and  in- 
crease the  activity  of  the  antagonistic 
centre. 


Fig.  29  illustrates  effects  of  lesions  of 
cauda  equina. 
Fig.  28  If  the  lesion  is  at  "A"  there  is  com- 

plete  motor  paralysis  of  both  legs,  and 
complete  anesthesia  of  the  whole  of  both 
legs    and    of    the    perineum,    buttocks, 
scrotum  and  penis,  and  all  reflexes  of  the 
legs  are  abolished. 
If  the  lesion  is  at  "B  "  there  is  complete  motor  paralysis  of  both  legs, 
except  the  flexors  of  the  thigh  and  the  extensors  of  the   leg,  and  complete 
anesthesia  of  the  perineum,  buttocks,    scrotum  and   penis,  and  of  the  pos- 
terior surface  of  the  thighs,  the  posterior  and  lateral  surfaces  of  the  legs,  and 
all  of  the  foot,  except  a  small  area  on  its  inner  surface.     All  the  reflexes  of 
the  legs  except  the  knee-jerks  are  abolished. 

In  both  cases  the  muscles  atrophy,  there  is  no  zone  of  hyperesthesia 
above  the  anesthesia  and  the  bladder  and  rectum  show  a  motor  and  sensory 
paralysis. 

If  the  lesion  is  limited  to  the  conus  medullaris  there  is  a  paralysis  of 
the  rectum  and  bladder  and  an  anesthesia  of  the  penis,  scrotum,  perineum. 
one  inch  about  anus,  and  the  upper  two-thirds   of  the   posterior  surface  of 
the  thigha      Otherwise  there  is  no  paralysis  of  motion  or  sensation. 
See  487,  721,  1007,  1308. 


D.XL 


Fio.  80 
Showing  the  inncrvaiion  of  muscles 
through  more  than  one  nerve  root,  so 
that  the  destruction  of  one  nerve  root  or 
of  OM  group  ol  iiitvo  cells  does  not  oauaa 
a  OOmpUta  and  permanent  paralysis. 


Fio.  31 
\  diagram  ahowina  that 
-tv  area  ol  the  skin  la  lappuM  l>y  Bla 

menta  from  several  nerve  roots;  so  that 
dividon  ol  one  root  does  not  necessarily 
produce  total  anesthesia.  It  alao  shows 
tho  peripheral  overlapping;  so  that  the 
upplied  by  ono  nerve  cun  bo  almost 
completely      supplied      I'.v     neighboring 


249 


Motor  and  Reflex  Functions  of  the  Spinal-Cord  Segments  (Modified 
after  Starr  and  Edinger) 


Segment 

Muscles 

Reflexes 

Cervical 

Sternomastoid 
Trapezius 

2-3         | 

Scaleni 

Small  rotators  of  head 

Diaphragm 

Lev.  ang.  scap. 

Dilatation  of  pupil  by  irri- 

Rhomboids 

tating  side  of  neck,  4  cer- 

4 

Spinati 
Deltoid 

vical  to  1  dorsal 

Supinat.  long 

Scapular  reflexes,  5  C-l  D 

Biceps 

Supinat.  long.,  5  C 

5 

Supinat.  brev. 
Serrat.  mag. 

Pectoralis  (clav.) 

Biceps,  5-6  C 

Teres  minor 

Triceps,  6  C 

Pronators 

Posterior  wrist,  6-8  C 

6' 

Brachialis  ant. 
Triceps 

Scapulo-humeral,  7  C 

Long  extensors  of  wrist  and 

Anterior  wrist,  7-8  C 

7 

fingers 
Pectoralis  (costal) 

Latiss.  dorsi 

Palmar,  7  C-l  D 

Teres  maj. 

|      , 

Long  flexors,  wrist  and  fingers 

Epigastric,  4-7  D 

Dorsal  1  1  1  { 

Extensors  of  thumb  1 

Intrinsic  hand-muscles 

Abdominal,  7-11  D 

2-12 

Dorsal  and  abdominal  muscles 

Lumbar 

Abdominal  muscles 

Cremaster,  1-3  L 

rH 

Iliacus 

Psoas 

Patellar,  2-1  L 

2 

Sartorius 
Flexors  of  knee 
Quad,  femoris 

Bladder,  2-4  L 

Int.  rotators  of  thigh 

f 

Adductors  of  thigh 

Rectal,  4  L-2  S 

4 

Abductors  of  thigh 

Tibialis  ant. 

Gluteal,  4-5  L 

f 

Calf -muscles 

5 

Ex.  rotators  of  thigh 

Extensors  of  toes 

Achilles,             1 1   **  S 
Ankle-clonus,    J 

Sacral 

Peronei 

"    \ 

Long  flex,  of  toes 

Plantar,  1-2  S 

Intrinsic  foot -muscles 

¥&>  }«■ 

3-5 

Perineal  muscles 

Fig.  32 


250 


251 


*V  VcSC-6vf.-Sp.naf  TVact 
V    RU«re-Spl«(T,att 
y  Tfcaf-^c   -Sp.xif    T.«.cT 

Fig.  34 


LONG  MOTOR  PROJECTION  TRACTS 
For  lesions  involving  these  tracts  see  under  Fig.  26. 

252 


Fig.  86 

LONG  SENSORY  PROJECTION  TRA<    Pfl 

For  lesions  involving  these  tracts  sec  umler  Fig,  28. 


263 


Tontfue 


Stylomastoid  foramen 
steriorAuruuIar 


Glosso  pharyngeal 


Fig.  36 

DIAGRAM  OF  TRIGEMINAL,  FACIAL  AND  GLOSSO-PHARYNGEAL  NERVES,  SHOWING 

COURSE  OF  TASTE  FIBRES. 

(After  Purves  Stewart) 


Optic  lUdlalioni 
Corpui  Calloiurn 

Optic  Thalamus 
Corp.  genlc  ext. 


Optic  Tract 
optic  Nerve 


Viaual  Word  Ceutre 
8 


Auditory   Word-Centre 


Fasciculus   IJorinatu* 


Vocal  Word-Centre 


mv> 


Fig.  37 
DIAGRAM  ILLUSTRATING  HEMIANOPIA 

(Modified  from  Vialet)  ...  , 

Lesion  at  1  produces  blindness  of  one  eye.  Lesion  at  5  produces  R.  hemianopia  with  normal  pupil  reaction. 

Lcaion  at  2  produces  bi-temporal   hemianopia  Lesion  at  0  produces  K.  hemianopia  with  normal  pupil  reaotion. 

Lesion  at  3  produces  bi-nasal  hemianopia  Lesion  at  7  produces  psychic  blindness. 

Lesion  at  4  produces  R.  hemianopia  with  hemiopic  pupil  reaction.  Lesion  at  8  produces  Alexia. 

The  heavy  black  lines  represent  the  fibers  from  the  macula  lutea  in  each  retina,  the  point  of  central, 

or  clearest  vision. 


254 


S    ES    ° 

3  fe  cp 
t*  £  £ 
fs  £  * 

-J 

J? 

!"vr 

fc: 
0. 

IS 

a?3 

pa 

5 

g 

z 

&: 

IP     L    UJ^i    $ 


k 


INDEX 


INDEX 


Roman   numerals   indicate   charts.         Arabic  numerals  indicate  margin  numbers. 
Arabic  numerals  preceded  by  "  p  "  indicate  pages. 


Abasia :     See   astasia 

Abdomen,   Boat-shaped   retraction   of,   XI, 

608 
Abdominal  spasm  or  cramp,  XII,  732 
.'  bducens  nucleus,  Conjugate   deviation  in 
lesions   near  the,  XIV,   883;   XXII, 
1328 

paralysis,  XII,  701 
Abductor  paralysis,  XIII,  756 
Abscess,  Cerebral :    See  cerebral 

Spinal :     See  spinal 
Abstraction,  p.   13 
Accommodation  reflex :     See  pupillary  and 

reflex 
Achilles  reflex,  I,  62;  V,  317 
Achillodynia,  XV,   1001 
Achondroplasia,  XVII,  1177 
Achromatopsia,   I,   13;   VI,  364;   XIV,  847 
Acromegalia,   I,  20;  XVII,  1183 
Acroparesthesia,  XVII,   1 197 
Action,  p.  21 

Association,  p.  22 

Autochthonous,  p.  28. 

Automatic,  p.  28 

Reflex:     See  Reflex 

Voluntary,  p.  22;   IV,  240 
Active  contracture,  IV,  264 
Acute  alcoholic  mania,  XVI,  1 109 

anterior    poliomyelitis :      See   poliomy- 
elitis 

or  apoplectiform   polioencephalitis 
inferior,    X,  544 
superior,  X,  543;  XVI,  1064 

ascending  paralysis,  II,   168;   X,  482 

ataxia:     See  ataxia 

atrophic  paralysis :      See   poliomyelitis 

bulbar  paralysis,  X,  544 

delirium,   XVI,   1108 

encephalitis,    multiple,    X,    495;    XVI, 
1064 
Adams-Stokes*  disease,  XI,  582;  XVI,  1057 

phrnomenon,  IX,  436 
Adiposis  dolorosa,  XV,   1012;   XVII,  1176 
Adiposogenital   degeneration,   XXI,   1279 
Adolescent  insanity,  XVI,  1096 
Aesthesiometer,  I,  48 
African  lethargy,  XVI,  1052 
Age  in  nervous  disease,  II,  86 

■<■  p.  7 ;  vi,  357 

Tests  for,  I,  17 
Agitated  dementia,  XVI,  1103 

melancholia,   XVI,    Ilia 
Agnosia,  p    i<>.  III.  -'.u 


Agoraphobia,    III,   235;   XVI,    1072 
Agraphia,  p.  28;  III,  227;  XIII,  "6 

localization  of,  XXI,  1282;  XXII,  1389 
Agrypnia,  I,  18 
Akinesia,  IV,  241 

Akinesthesia,  I,  42;  VI,  352;  XIV,  812 
Albinism,  XII,  683 
Alcoholic   coma,   XVI,    1053 

convulsion,  XI,  576,  585 

dementia,   XVI,  1101 

hallucinosis,  XVI,  1 109 

headache,  XV,  953 

intoxication,  XII,  658,  663,  673;  XIII, 
764,  780 

mania,  Acute,  XVI,  1107,  1109 

neuritis,    X,   488 

tremor,   XII,   673 

vertigo,  XV,  1030 
Alcoholism,  I,  2;  II,  115;  XII,  658;  XIII, 

-64,  780 
Alexia,  p.  28;  III,  228;  XIII,  773 

Localization  of,  XXII,  1391 
Allocheiria,  VI,  377 
Alopecia,  XVII,  1161 
Altruism,  p.  16 
Amaurosis,  VI,  358 

Uremic,  XIV,  850 
Amaurotic  idiocy,   XVI,   1085 
Amblyopia,  VI,  359;   XII,  682 

Hysterical,  XIV,  851a 
Ambulatory  automatism,  XVI,  1058,  1069-71 
Amentia,  p.  19;  III,  211 

Diseases  causing,  XVI,  1076 
Amnesia,   I,  6;   III,  220;  XIII,  770 

Retroactive,  XIII,  769;  XVI,  1 100 

Retrograde,  XIII,  769 
Amyl  nitrite  poisoning,  XIV,  842 
Amyotonia  congenita,   II,   105;   X,  4^.1 
Amyotrophic  lateral  sclerosis,  X,  54;;  XII, 

695;  XIII.  797;  XVII,  1149 
Anakusia,   VI,   355;   XIV,  820 

Diseases  causing,  XIV,  820 

Tests  for,  I,  15 
Ana'   reflex,  V,  307a 
Analgesia,  VI,  349 

Diseases  causing,  XIV,  810;  XXII,  1341 

Tests  for,  I,  50 
Anarthria,  p.  a6;    IV.   jS*  ;   XIII,  737,  771 

Disease*  causing,  XIII,  737 

literalis.   XIII.   r<  7 

spasmodica,    XIII.    j6t 
Anemia,  Cerebrospinal  fluid  in,  XIX.  1343 


850 


INDEX 


Anemic  convulsion,  XI,  583 
headache,  XV,  949,  958 
optic  neuritis,  XIV,  902 
vertigo,  XV,  1021-5 
Anesthesia,  p.  7;  VI,  348;  XIV,  810 

Diseases    causing,    XIV,    810;    XXII, 

1340 
dolorosa,  VI,  374 
Glove  form  of,  VI,  34s ;  IX,  425 
Hysterical,   p.    7;    VI,   345;    IX,   425; 

XIV,  834 
of   larynx,  XIII,  754.  7°o-I 
Localization  of,  XXII,  1340 
Stocking  form  of,  VI,  345 ;  IX,  425 
Tests  for,  I,  48 
Thermic,  VI,  350 ;  XIV,  810 
Tests  for,  I,  55 
Aneurism,   Cerebral,  X,  502 
Angina  pectoris,  XV,  983 
Anginal  crises,  IX,  433 
Angio-neurotic   edema,    XVII,    1201 
-paralytic  hemicrania,  XV,  949 
-sclerotic  dysbasia,  X,  554;  XVII,  1 199 
-spastic  hemicrania,  XV,  949 
hemiplegia,   X,   554 
Angular  gyrus,    Symptoms   of    lesions   of, 

XXII,  1391 
Anisocoria,  I,  26;  V,  341 
Ankle-clonus,  V,  316 
Tests  for,  I,  60 
Ankylosis,  Tests  for,  I,  37 
Anopsia,  VI,  358 
Anosmia,  VI,   356 

Tests  for,  I,  16 
Anterior  central  convolution :     See  localiz- 
ation 
commissure  of  cord:     See  localization 
crural   neuralgia  or  neuritis,   XV,  997 
horn   or  column  or  nerve   root:     See 
spinal  cord 
Apallesthesia,  VI,  353 

Tests   for,  I,  56 
Apathetic  dementia,  XVI,   1095,   1103 
Apathy,   III,   237 
Ape's  hand,  XII,  714 
Aphasia,  I,  6;  III,  221;  XIII,  739 
Auditory,  pp.  10,  28;  XIII,  772 
Conduction,  p.  28,  XIII,  739 
Cortical  motor,  XIII,  739 

sensory,  XIII,  739 
Diseases  causing,  XIII,  739 
Mixed,   III,  224;   XIII,   774 
Motor,  III,  221 ;  XIII,  771 

Localization  of,  XXI,  1282;  XXII, 
1390 
Optic,  IN,  223;  XIII,  773 
Sensory,   pp.    10,    28;    I,   6;    III,   222; 
XIII,  772 
Localization  of,  XXI,  1284;  XXII, 
1345 


Aphasia,  Sub-cortical  motor,  XIII,  739 
sensory,  XIII,  739 
Trans-cortical  motor,  XIII,  739 

sensory,  XIII,  739 
Visual,  III,  223;  XIII,  773 
Aphemia,  XIII,  771 
Aphonia,  IV,  260;  XIII,  744,  754,  756-60 

Hysterical,  XIII,  747-8,  759 
Aphthongia,   XII,  729;   XIII,  767 
Apoplectiform     polioencephalitis     inferior, 
X,  544 
superior,  X,  543 
Apoplexy,  II,  186 

Athetosis  after,  X,  503;  XI,  631 
Cerebral,  X,  504;  XI,  588;  XIV,  832; 

XVI,  1043,  1061-3 
Ingravescent,  XVI,  1060-3 
Meningeal,  X,  502,  524;  XI,  588;  XVI, 

1060 
in   pons   Varolii,   XIII,   748a 
Prodromata  of,  IX,  432 
Vertigo  from,  XV,  1026 
Apraxia,  pp.  26-7;  III,  230;  IV,  249,  282; 
XVI,  1 104 
Association,  p.  27 
Motor,  p.  27 
Aran-Duchenne  type  of  muscular  atrophy, 
X,  547;  XII,  694;  XIII,  797;  XVII,  1149 
Arcus  senilis,  I,  24 

Argyll-Robertson's  pupillary  reflex,  V,  332; 
IX,  447 
Diseases  causing,  XIV,  891 
Arm-center,     Symptoms     of     lesions     of, 
XXII,   1349,  1352,   1369,   1376,   1379.   1381 
Arsenical  neuritis,  II,   157;  X,  488 
Arterial    disease    in    etiology    of    nervous 

diseases,  II,  97 
Arthralgia,  XV,  1000 
Arthritic  atrophy.   XVII,   1151 
Arthritis  deformans,  XV,  976 
Arthropathy  of  tabes,  XVII,  1186 
Articulative  tics,  XIII,  768 
Asphyxia,  Local,  XVII,  1 195 
Associated  movements,  IV,  276 
Association  of  ideas  and  memories,  p.   12 

Tests  for,  I,  5 
Association  reflexes,  pp.  22-3 
Astasia    and    abasia,    IV,    287;    XII,    653; 

XIII,  792 
Astereognosis,   p.    10;    III,    229;   VI,   354; 
XXII,  1346,  1369 
Tests  for,  I,  11 
Asthenic  tremor,  XII,  671 
Asthma,  XI,  617;  XVII,  1194 
Astrophobia,  III,  235 
Asynergia,  p.  26;  IV,  248 
Ataxia,  p.  26;  I,  21,  41;  III,  248;  X,  488; 
XII,  638;   XXI,   1268-73 
Acute,  X,  488;  XII,  659,  662 
Aural,  XII,  650 


260 


INDEX 


Ataxia,   Diseases   causing,   XII,  638 
Dynamic,  p.  26;  IV,  280;  XII,  644 
Cerebellar,  p.  26;  I,  21;  IV,  281;  XII, 

642;  XXI,  1268-73,  1282 
Cerebral,    p.    26 
Friedreich's    hereditary,    II,    104,    123 ; 

XII,  652,  670,  687,  XIII,  762,  781 
Hysterical,  XII,  664 
Locomotor :     See  tabes 
Marie's  hereditary  cerebellar,  XII,  651, 

669;  XIII,  782 
Motor,  p.  26;  I,  21;  IV,  280;  X,  488; 

XII,  644;   XXI,   1268-74 
Ocular,  XII,  649 
Post-hemiplegic,   XII,   655 
Static,  p.  26;  IV,  281;   IX,  448;   XII, 

Vertigo  with,   XV,   1015 
Ataxic   gait,    Diseases    causing,    XIII,    740 
paraplegia,  X,  526;  XII,  660;  XIII,  796 
Ateleiosis,  XVI,   1093 
Atheromatous  arteries,  Vertigo  from,  XV, 

1025 
Athetoid  spasms,  Diseases  causing,  XI,  574 
Athetosis,  I,  32;  IV,  271;  X,  501,  503 
after  apoplexy,  X,  507;  XI,  631 
in  cerebral  palsy  of  childhood,  X,  501 ; 

XI,  630 
Congenital,  X,  501 ;  XI,  629 
Athlete,   Muscular   hypertrophy   in,    XVII, 

"54 
Atonia,  I,  39;   IV,  240 
Atonic  paralysis,  I,  39;  IV,  252;  X,  472 
Atrophic  paralysis,  IV,  252;  X,  472,  547 
Atrophies,  Degenerative,  X,  476 

Localized,  XVII,  1188 
Atrophy,  Arthritic,  XVII,   1 126,   1151 

of  bone,  Diseases  causing,  XVII,  1138 
fat.  Diseases  causing,  XVII,  1136 
muscles,  Diseases  causing,  I,  40,  X, 

476-7;  XVII,  1 130 
skin,  Diseases  causing,  XVII,  1132 
Attention,  p.  13 

Tests  for  power  of.  I,  5 
Attitudes  passionellcs,  XI,  586 
Auctioneer's  cramp,   XII,  726 
Audition,  Cortical  center  of,  p.  8 
Auditory  aphasia,  p.  10;  XIII,  772 

nerve,   Deafness  in   atrophy   of,    XIV, 
919 
Electric  reaction  of,  VII,  405 
Lesions  of,  XIV,  920 
■enaction,  p.  8 
Aura  of  epilepsy,  IX,  430 

Glittering  scotoma  as,   XIV,  846 
of  migraine,  rlemianopia  as,  XIV,  854 
Aural  ataxia.   XII,  650 

vertigo,  XII,  650,  6B5;   XIV,  018;  XV, 
1019 
Autochthonous   acts,   p.   28 


Automatic  acts,  p.  28 

Automatism,  III,  210 

Ambulatory,  XVI,  1058,   1069-71 
Diseases  causing,   XVI,   1039 
Epileptic,    XI,    575;    XVI,    1058 

Auto-suggestion  in  hysteria,  IX,  4_'5 ;  XVI, 
1069-71 

Auto-toxic   coma,   XVI,   1067 
convulsions,  XI,  596 

Avelli's  syndrome,  XII,  706 

Awkwardness :     See   apraxia 

Axillary  paralysis,  XII,  712 

Axon,  p.  5 

Babinski  and  Nageotte's  bulbar  syndrome, 

IX,  437;  XXI,  1268 
Babinski's  associated  movements  of  trunk 
and  thigh,  IX,  446 
reflex,  V,  304 

Tests  for,  I,  57 
Backache,  Diseases  causing,  XV,  935 
Barlow's  disease,  X,  495 
Basedow's  disease.   XII,  672;   XVII,    1193 
Bathyesthesia,  I,  42 

Bechterew's  reflex :    See  dorsal  foot  reflex 
Bed  sores,  XVII,   1171 
Bell's  palsy,  XII,  703 

phenomenon,  IX,  444;   XII,  703 
Benedykt's  syndrome,  IX,  441 ;  XXI,  1270 
Beri-Beri :     See  neuritis,  multiple 
Bewildered  mental  condition,  III,  207 
Biernacki's  sign,  IX,  449 
Binocular  diplopia,  VI,  383;  XIV,  816 
Biot's  respiration,  IX,  435 
Bitemporal  hemianopia,  VI,  362;  XIV,  815, 

860,  892;  XII,  1319 
Bladder  reflex,  V,  323 
Blepharospasm,  XI,  601,  617;  XII,  682,  726 
Blindness,    VI,    358;    XIV,    850-1;    XXII. 
1318 
Color,  VI,  364 
Diseases  causing,  XIV,  815 
Psychic,    III,   232;    XXI,   1285;    XXII. 

1344 
Snow.  VI,  360;  XIV,  843 
Word,  III,  228,  233;  XIII,  773 
Boat-shaped    retraction    of    abdomen,    XI, 

608 
Bone,  atrophy  of,  Diseases  causing.  XVII. 
11.  iS,    117.) 
conduction,  Tests  for,  I,  15 
Fragility  of,  XVII,  1140,  1185 
Hypertrophy     of,     Diseases     ctnaing, 

XVII.  1x39 
tissue,    trophic     lesions    of,    Diseases 
canting,  xvn.  1  u; 
Boiton  ECocher'a  rign,  XVII,  1192 
Rrachycephali.i 

Brachial   plexus.    Neuritis  or  injury  of,   X. 
400 


.-■< 


INDEX 


Brachial   plexus,   paralysis,    IX,   454-5;    X, 
490;   XXII,   1306 
Sjasm  or  cramp,  XII,  733 
Symptoms    of    lesions    of,    XXII, 
1306 
Bradycardia,  XII,  728 
Brain  puncture,   I,  75 

stem,  Definition  of,  IX,  460 

Hemorrhage,      inflammation,       or 

softening  in,  X,  535;  XII,  656 
Lesions  of,  XIV,  830;  XV,  1017 
Localization  in  :     See  localization 
Symptoms  of  lesions  of  the,  XXII, 
1301-4,   1375,   1378,   1382-4;   1388. 
1398 
Tumor  of  the,  X,  536;  XII,  656 
Vertigo  in  lesions  of,  XV,  1017 
Bright's  disease,  Optic  neuritis  in,  XIV,  899 
Brown-Sequard  paralysis,  IX,  442;  X,  509; 

XIV,  840;  XV,  981 
Brudzinski's  neck  sign,   IX,  456 

leg  sign,  IX,  457 
Bulbar    paralysis,    IX,    434;    X,    544,    546; 
XII,  694;  XIII,  756,  761;  XVII, 
1 150 
Acute,  X  544 
Chronic,  X,  546;  XII,  694;  XVII, 

1 150 
Progressive,    X,    546;    XII,    694; 

XVII,   1150 
Pseudo-,  X,  553 
Symptoms  of,  IX,  434 
Burdach's  column :     See  spinal   cord 

Caisson  disease,  X,  521 
Calcanodynia,  XV,  1002 
Calcarine  fissure,  Symptoms  of  lesions  of, 

XIV,  847,  852-3,  855-6;  XXII,  1364-6 
Caloric  reaction,  I,  79;  XII,  685 
Cannabis  Indica  poisoning,  XIV,  842 
Capsule,  External :     See  external 

Internal:     See   internal 
Caput  obstipum  paralyticum,  XII,  705 

spasticum,  XII,  705,  730 
Cardiac  disease,  Vertigo   from,  XV,  1024 
Caries  of  the  spine,  II,  121 
Case  taking,  I 

Casque  neurasthenique,  XV,  959 
Catalepsy,  XI,  611;  XVI,  1096-8 
Cataract,  Diplopia  in,  XIV,  880 

operation,    Perversion  of  vision   after, 
XIV,  843-4 
Catatonia,  XVI,   1098 

Cauda  equina,  Paralysis  of,  X,  487 ;  XII, 
721 
Symptoms  of  lesions  of,  X,  487; 
XV,  1007;  XXII,  1308 
Central  convolution,  anterior,  Symptoms  of 
lesions  of,  XXII,  1373,  1376, 
I379-8I,  1387;   1400-5 


Central    convolution,   posterior,    Symptoms 
of     lesions    of,     XXII,     1348-9, 
1352,  1369 
motor  neurons,  IX,  461 

Diseases  of,  IX,  473,  XVII,  1153 
Location  of  lesions  of,  XXII,  1293 
sensory  neurons,  IX,  463 
Cephalalgia:     See  headache 
Cerebellar  artery,  posterior  inferior.Throm- 
bosis  of  the,  XXI,  1268 
ataxia,  IV,  281;  XII,  642,  669;  XXI, 
1268-74,   1282 
Diseases  causing,  XII,  642 
Marie's  hereditary,  XII,  651,  669; 

XIII,  782 
mystagmus,  I,  80 

peduncles,    Symptoms    of    lesions    of 

the,  XXI,  1273 
tract  (direct),  Lesion  of  the,  XII,  654; 
XXII,   1356,  1360 
Cerebellum 

Diseases  of  the,  XII,  686 
vertigo  in,  XV,  1016 
Lesions  of  the,  XII,  648;  XIII,  783; 
XXI,  1272 
vermis  of  the,  XI,  610 
hemispheres  of  the,  XI,  609 
Localization   in  :     See  localization 
Cerebral  abscess,  II,  152,  181;  X,  508;  XI, 
578,  587;   XIV,  907;   XV,  960; 
XVI,  1046 
Cerebro-spinal  fluid  in,  VIII,  411; 

XIX,  1237 
Headache  in,  XV,  960 
activity,    Diseases    causing    weakened, 

XVI,    1040- 1 
anemia,  Vertigo  from,  XV,  1021-5 
aneurism,  X,  502 

apoplexy :     See  hemorrhage  and  soft- 
ening 
compression,   XVI,   1042 
concussion,   XVI,   1043 
congestion,  XV,  957,   1025a 
contusion,  XVI,  1043 
cortex,    Symptoms   of   lesions   of   the, 
XXI,  1286 
Conjugate  deviation  of  eyeballs  in 
the     irritative     lesions    of     the, 

XIV,  817 
cyst:     See  tumor 
decompression,  XV,  960 

diplegia,   X,  478,  501;   XI,  577;   XIII, 

798;    XVI,    1048 
disease,  XII,  689 
edema,    Cerebro-spinal    fluid   in,   VIII, 

411 
embolism,  X,  505 ;  XIV,  832 ;  XVI,  1062 
endarteritis,   Syphilitic,   XVIII,   1207 
gumma,  Isolated,  XVIII,  1206 


262 


INDEX 


Cerebral  hemorrhage,  II,  146;  X,  503;  XI, 
588;  XIV,  832,  856-7;  XVI,  1043. 
1061 
Cerebro-spinal      fluid      in,      VIII, 

41 1-3;   XIX.I240 

into  ventricles,  X,  504 

localization :      See    localization 

meninges :     See   hemorrhage 

meningitis:     See  meningitis,  cerebral 

Cerebro-spinal  fluid  in,  VIII,  410; 

XIX,   1226-9,   I239 
Headache  in,  XV,  961,  964 
palsy   of   childhood,   II,    116;    X,   501; 
XI,  577,  630;  XIII,  798;  XVI,  1048, 
1086 
softening,  X,  505-6;  XIV,  832;   XVI, 

1062-3 
syphilis,   XVIII,   1206-9 

Cerebro-spinal  fluid  in,  VIII,  410; 
XIX,  1230-2 
thrombosis,  X,  506 ;  XVI,  1063 ;  XVIII, 

1207 
tumor,    II,    151;    X,    507,    536-42;    XI, 
578,  587;  XIV,  833,  849.  855-61, 
892;  XV,  908,  960;  XVI,  1047 
Cerebro-spinal  fluid  in,  VIII,  411, 

419;  XIX,  1236 
Headache  in,  XV,  960 
Optic  neuritis  in,  XIV,  908 
Perversion  of  vision  in,  XIV,  849 
Vertigo  from,  XV,  1032 
Cerebration,   Disturbances  of,  III,  200 
Cerebro-spinal  fluid,  p.  29;  I,  74 

Abnormal,  VIII,  410;  XIX,  1220 

in  abscess,  XIX,  1237 

Albumen  in,  VIII,  418 

in  anemia,  XIX,   1242 

Bacteria  in,  VIII,  416;  XIX,  1223-4 

Blood  in   the,  VIII,  412-3;   XIX, 

1225 
Butyric  acid  test  in  the,  VIII,  419; 

XIX,    1221-2 
Cellular  elements  in  the,  VIII,  416 
in  cerebro-spinal  meningitis,  XIX, 

1226 
clear    with    coagulum,    VIII,   415; 

XIX,  1223-4 
cloudy.  VIII,  414:  XIX,  1223 
in   epidemic  cerebro-spinal  menin- 
gitis. XIX.  1  '-•'■ 
Examination  of  the,   I,  74;  VIII, 

410 
Globulin  in  the,  VIII,  410 
in  hemorrhage  in  cerebral  or  spinal 
meninges  or  in  ventricles,  XIX, 
i.- 1' 1 
in   herpes   zoster,   1234 
in  hydrocephalus,  XIX.  [338 
Leucocytosis   in,    V11I,   416;    XIX. 
1 -'-'3 


Cerebro-spinal     fluid,     Lymphocytosis     in, 
VIII,  416;   XIX,   1224 
in  meningitis,  VIII,  410;  XI,  590; 

XVIII,  1214,  1226-9,  1239 
Noguchi    test    in    the,    VIII,    419, 

XIX,  1221 
Obtaining  of,  I,  74 

in  paresis,  VIII,  420;  XIX,  1230 
poliomyelitis,    VIII,   416,   419; 

X.  495;  XIX,  1233 
purulent  meningitis,  XIX,  1227 
Red  or  reddish  color  of  the,  VIII, 

412-3 
in  serous  meningitis,  XIX,  1238 
sporadic  purulent  meningitis,  XIX, 

1227 
Sugar  in,  VIII,  417 
in  syphilis,  VIII,  410;  XVIII,  1214 

tabes,  VIII,  420;  XIX,  1231 
Tension  of  the,  VIII,  411 
in  tumor  of  brain  or  spinal  cord, 
XIX,  1236 
typhus  fever,  XIX,  1235 
tuberculous    meningitis,    XIX, 

1228-9 
uremia,  XIX.   1241 
Wassermann  test  in  the,  VIII,  420; 
XIX,  1224 
Cerebro-spinal   syphilis,   XVIII,    1214 
Cervical    region    and    enlargement :      See 
spinal   cord 
rib    pressing    upon    subclavian    artery, 

X,  556 
sympathetic,    Irritation   of   the,   XVII, 
1 192 
Paralysis  of  the,   XVII,   1191 
Cervico-brachial  neuralgia,  XV,  995 
Charcot's  disease,  XVII,  1186 
Charcot- Marie-Tooth's    type    of    muscular 

atrophy,  X,  496;  XII,  696 
Chasmus,  XII,  731 
Cheyne-Stokes'  respiration,  I,  4?;  IX,  435; 

XII,   728;   XXI,   1268 
Chills.  XII,  680 

Choked  disc,   Diseases  causing,    XIV,  897 
Chondrodystrophia  foctalis,  XVII,   1177 
Chorea,  II,   11 2.   iaSi   IV,  272;   V 
Degenerative.    XI,  624 
Electrical,   XI,   600,  627 
gravidarum,  XI,  622 
Hal.il.    IV.    .7. 1  ;    XI,   626 
Hcnii-.   IV,   27a;   X,  510 
Hereditary,  II,  103;  XI 
Huntington's,  11,  103;   \ 
Hysterical,  XI,  628 
Infectious,  X 

major  or  m.iRna,   IV,  273;   XI. 
minor.    IV.   . 
mollis,   X,  5:0 


263 


INDEX 


Chorea,  in  pregnancy,  XI,  622 

Rhythmical,  XI,  628 

Senile,  XI,  624 

Sydenham's,  XI,  622 
Choreic  movements,  I,  32;  IV,  272 

paralysis,  X,  510 
Choreiform  spasms,  Diseasescausing,  XI, 573 
Chvostek's  sign,  IX,  451 ;  XI,  614 
Chromatopsia,  Tests  for,  I,  13 
Chronic   atrophic   paralysis,   X,    547;    XII, 
694;  XIII,  797;  XVII,  1 149 

bulbar    paralysis,    X,    546;    XII,    694; 
XVII,   1 150 
Cilio-spinal  center,  IX,  465 

reflex,  V,  335 
Circular   insanity,   XVI,   1 116 
Circulation,  Tests  for,  I,  45 
Circulatory,     disturbances,    Perversion    of 

vision   in,   XIV,  845-6 
Claudication,  Intermittent,  X,  554;  XVII, 

1199 

Claustrophobia,  III,  235;  XVI,  1072 

Claustrum  and  external  capsule,  Symptoms 
of  lesions  of,  XXI,  1278 

Clavus,  XV,  950 

Claw-hand,  X,  547;  XII,  715 

Cleft  palate,  XIII,  749 

Clitoridian  crises,  IX,  433 

Clonic  spasm,  IV,  246 

Diseases  causing,  XI,  571 

Clubbed  fingers  and  toes,  XVII,   1 184 

Coal  gas  poisoning,  XVI,   1055 

Coccygodynia,  XV,  972 

Coffee  vertigo,  XV,  1030 

Cold  as   etiological   factor,  II,   100 

Colic,  Lead,  II,  158;  XV,  988 

Color  blindness,  VI,  364 

fields,    Interlacing,    and    inversion    of, 

I,  14;  XIV,  849 
sense,  Tests  for,  I,  13 

Coma,    I,    3;    HI,   205;    XIII,    745 ;    XVI, 
1037 
Alcoholic,  XVI,  1053 
Diabetic,  II,  190;  XVI,  1065 
Diseases   causing,   XVI,    1037 
Epileptic,  XI,  575;  XVI,  1058 
Hysterical,  XVI,   1069 
in  internal  hemorrhage,  XVI,  1056 
pseudo-,   Diseases   causing,   XVI,   1038 
Toxic  or  Auto-toxic,  XVI,  1067 
Uremic,  XVI,   1066 
Vigil,  III,  206 

Comprehension,  Tests  for  power  of,  I,  5 

Compression   of   brain   stem,   X,   536,   538, 
540,  542 
Cerebral,   XVI,    1043 
myelitis,  II,   121;  X,  520;  XIII,  795 
neuritis,   XV,  939 
Compulsory  acts  and  ideas,  I,  4;  III,  218; 
IV,  275 


Concentration,  p.   13 

Concentric  limitation  of  field  of  vision,  IX, 

425;   XIV,  815 
Concepts,  pp.   10,   13 
Concussion,  Cerebral,  XVI,  1042 
Conduction  of  pain,  Retardation  of,  I,  S1  > 
VI,  381 
of    motor   impulses,   p.   24 
sensory  impulses,  p.  6  et  seq. 
Confusional  insanity,  XVI,   1106 
Congenital  dislocation  of  hip,  XIII,  786a 
Congestive  headache,  XV,  957 
Conjugate    deviation    of    eyeballs,    Lesions 

causing,  XIV,  817 
Conjunctival  reflex,  V,  312 

Tests  for,  I,  58 
Consanguineous      marriages     in     nervous 

diseases,    I,   2 ;    II,   81 
Conscience,  p.  13 
Consciousness,  p.  15 

Disturbances  of,  I,  3 ;  III,  201 
Consensual  pupillary  reflex,  I,  25 
Constipation  headache,  XV,  955 
Continous   paralysis,   Diseases   causing,   X, 

470 
Contraction,  Fibrillary,  IV,  292;  XII,  641 
Contracture,  Active,  I,  38;  IV,  264 
Dupuytren's,  XI,  620 
Hysterical,    XI,   618 
Passive,  I,  38;  IV,  263 
Post-hemiplegic,  X,  504;   XI,  577,  619 
Post-neuritic,  XI,  621 
Post-paraplegic,    X,    480,    548-5 1 ;    XI, 

620 
Tests  for,  I,  32,  38 
Contusion,  Cerebral,  XVI,   1043 
Conus-terminalis  of  spinal  cord,  lesion  of, 

XIV,  830a 
Convergence,  Deficient  and  cyclopegia,  V, 

331 
Conversation  in  diagnosis,  I 
Convulsions,   p.   25;    IV,   269;   XI,   570-1; 
XVI,  1037 
Alcoholic,  XI,  576,  585 
Anemic,  X,  583 
Auto-toxic,  XI,  596 
Diseases  causing,  XI,  571 
Epileptic,   XI,  575;   XVI,   1058 
Febrile  or  toxic,  XI,  595-6 
Hysterical,  XI,  586 
Lead,   XI,    584 
Location    of    lesions    causing,    XXII, 

1291 
Strychnine,  XI,  615 
Tests  for,  I,  32 
Toxic  or  febrile,   XI,  595 
Uremic,  XI,  576,  581 
Convulsive    tics,    IV,    267,    270;    XI,    601, 
617;  XII,  726 


264 


INDEX 


Coordination,  Tests  for,  I,  41 

Coprolalia,  XVI,  1096-8 

Cornea,   Diplopia  in    irregularities  of   the, 

XIV,  882 
Corneal  reflex,  I,  58;  V,  312 

Tests  for,  I,  58 
Cornet  players'  cramp,  XII,  726 
Corpora    quadrigemina,     Localization     in : 

See   localization 
Corpus  callosum,  Symptoms  of  lesions  of, 
XXI,  1277 
Striatum,  Localization  in  :    See  localiz- 
ation 
Cortical  lesions :     See  localization 
Cramp,  XI,  616;  See  also  spasm 
Cranial  asymmetry,  I,  22 
fontanelles,  I,  22 
hyperostosis,  XVII,   1181 
nerves :    See  nerves 
nuclei :     See   nuclei 
sutures,  I,  22 
tumors,    I,    22 
Cranium,   base    of,    Localization   of:      See 

localization 
Creative  faculty,  p.  14 
Cremasteric  reflex,  V,  308 

Tests  for,  I,  57 
Cretinism,   XVI,    1090;    XVII,   1164 
Crico-arytenoid   posterior   paralysis,   XIII, 

756 
Crico-thyroid  paralysis,  XIII,  754 
Criminals,   Habitual,   XVI,   1094 
Crises,  Tabetic,  IX,  433 
Crossed  hemianesthesia,  VI,  345 

paralysis,    IV,    256;    X,    537-42;    XV, 
1017;  XXI,  1268-70 
Croup,  Spasmodic,  XI,  617;  XII,  728 
Crura    cerebri,    Hemorrhage    or    softening 
in  the,  X,  537 
Localizing  symptoms  in  the :     See 

localization 
Symptoms  of  lesions  of  the,  XII, 
676;  XXII,  1324,  1329,  1384,  1398 
Tumor  in  the,  X,  538 
Crural  neuralgia,  XV,  997 

paralysis,  XII,  717;  XV,  997 
Cutaneous     eruptions,     Diseases     causing, 
XVII,   1134 
reflex  acts,  V,  297 

Tests  for,  I,  57 
sensibility,  p.  6 

tissue,  atrophy  of,  XVII,  1132 
Hypertrophy  of,  XVII,  1133 
trophic   lesions,    Diseases   causing, 
XVII,    1123 
ulcerations,    Diseases    causing,    XVII, 

1X35 

Cyanosis,  Local,  XVII,  1193 

Cycloplegia,  V,  331 

Cyst,  Cerebral :     See  tumor 


Dazed  mental  condition,  III,  207 
Dead  fingers,  XVII,  1195 
Deaf-mutism,  XIII,  744 
Deafness,  p.  8;  VI,  355;  XIV,  820 
Diseases  causing,  XIV,  820 
Hysterical,  XIV,  924 
Psychic,  p.  10;  III,  222,  233;  XIII,  ^2 
Tests  for,  I,  15 
Decompression,  cerebral,  XV,  960 
Decubitus,  XVII,  1171 
Deep  reflex  acts,  I,  60-6;  V,  299 

sensibility,  p.  6 
Defectives,  p.   19;  XVI,  1093 
Degeneration,   Electrical  reaction  of,  VII, 

399,  400,  404 
Degenerative   atrophies,   X,  476 

chorea,   XI,  624 
Deliberation,  p.  23 
Delirium,  p.  20;  III,  217 

Acute  or  grave,  XVI,  1108 
tremens,  XVI,  1107 
Delusional     insanity,     XIII,     746;     XVI, 
1 109-13 
Diseases  causing,  XVI,   1079 
Delusions,  p.  20;  I,  4;  III,  215 
in   hysteria,   IX,   425 
of  grandeur,  XVI,   11 13 
observation,  XVI,  11 13 
persecution,  XVI,  11 13 
Dementia,  p.  19;  III,  212;  XIII,  770 
Agitated,  XVI,   1103 
Alcoholic,  XVI,   1101 
Apathetic,  XVI,  1095,  1103 
Diseases   causing,    XVI,    1077 
Epileptic,  XI,  575;  XVI,  1102 
Paralytic :    See  paresis 
precox,   XVI,    1096 
Primary,  XVI,  1095 
Secondary,  XVI,  1 103 
senilis,    XVI,    1105 
Terminal,  XVI,  1103 
Demoniacal  possession,  p.  18 
Dendroni,  p.  5 

Dercum'i  disease,  XV,  1013;  XVII,  1176 
Dermographia   I,  59;  V,  326;  XVII,  n<>7, 

1200 
Deviation  of  the  eyeballs,  conjugate,  Dis- 
eases causing.  XIV,  817 
Secondary,  of  sound  eye,  I,  29;  XIV, 
816 
Tests  for,  I,  29 
Diabetes  mellitus,  Coma  in,  II,  190;  XVI, 
1065 
Fat  atrophy  in,  XVII,  117s 
( >|>tii-  neuritis  111.  XIV,  900 
Perforating  ulcers  in,   XVII,   1172 
I tiadoookynctU,  IV,  288 
Tests  for,  I,  36 


»6S 


INDEX 


Diagnostic  charts.     Introduction  to,  p.  1 19 
Diaphragm,  Paralysis  of,  XII,  707 
Digestive    disturbances,    Vertigo    in,    XV, 
1023 
perversion  of  vision  in,  XIV,  845 
Diphtheritic  paralysis,  X,  488;  XIII,  753-4 
Diplegia,  IV,  478;  X,  478;  XII,  703 
Cerebral :     See  cerebral 
Infantile :    See  infantile 
Diplopia,  I,  24,  28;   XIV,  816 
Binocular,  VI,  383;  XIV,  816 
Diseases  causing,  XIV,  816 
Hysterical,  XIV,  878 
Monocular,  VI,  384 ;  XIV,  816 
Tests   for,   I,  28 
Displacement  of  eyeball,  XIV,  877 
of  lens,  XIV,  881 
of  visual  axis,  I,  28;  XIV,  816 
Disseminated    myelitis    or    sclerosis:      See 

sclerosis 
Dissociation   of   sensation,  VI,  365 ;   XIV, 
811 
Diseases  causing,  XIV,  811 
Disuse,    Bone    atrophy    from,   XVII,    1178 
Diver's  paralysis,  X,  521 
Dolicocephalia,   I,   22 
Dorsal  foot  reflex,   I,  63 ;   V,  320 

region  of  cord :     See  spinal  cord 
Double  personality,  III,  209;  XVI,  1039 
Diseases  causing,  XVI,   1039 
pupillary  opening,  XIV,  879 
sensation,  VI,  378 

Tests  for,  I,  54 
vision :     See  diplopia 
Drug  habit,  I,  1,  2;  X,  482;  XII,  663 
poisoning,   II,  164 
vertigo,  XV,   1030 
Drunkenness  in  nervous  diseases,  I,  2;  II, 

"5 
Dubini's  disease,  XI,  600,  627 
Dupuytren's  contracture,  XI,  621 
Dwarfism,  XVII,  1164,  1177 
Dynamometer,  Testing  with,  I,  34 
Dysarthria,    p.    28;    I,    8;    IV,   284;    XIII, 
738 
Diseases  causing,  XIII,  738 
Localization    of,    XXI,    1276;    XXII, 
1375,    1378,   1382-3,   1388 
Dysbasia   angio-sclerotica,    X,   554;    XVII, 

1 199 
Dyschromatopsia,  I,  14;  XIV,  849 
Dysmasesis,  IV,  286;  X,  553 
Dyspepsia,    Headache  in,   XV,   952 
Dysphagia,  IV,  285 

Localization     of,     XXII,     1375,     1378, 
1382-3,  1388 
Dyspinelismus,   XXI,    1280 
Dystrophies,    Muscular,    II,    107,    127;    X, 
477;  XIII,  786;  XVII,  1152 


Ear  disease  as  cause  of  headache,  XV,  952 
Deformity  of,  XVI,  1076 
Hyperemia  of  inner,  XIV,  927 
Lesion  of,  XIV,  921,  927 
Echolalia,  XVI,  1096-8 
Echopraxia,  XVI,  1096-8 
Eclampsia,  XI,  576;  XVI,  1059 
Edema  angio-neurotica,  XVII,   1201 

Localized,  of  scalp,  XVI,  1044 
Ego,  The,  p.    16 
Egotism,  p.  16 
Elbow  reflex,  V,  321 

Tests  for,  I,  64 
Electrical  chorea,  XI,  600,  627 

motor  points,  I,  70;  VII,  395;  Vllb 
reaction,  I,  70-1 ;  VII,  395 

of  auditory  nerve,  VII,  405 
of  degeneration,  VII,  399,  400,  404 
Diminished,  VII,  397 
Exaggerated,  VII,  398 
formula  of  degenerated  nerve  and 
muscle,  VII,  399 
of   normal  nerve   and   muscle, 
VII,  396 
of  muscles  and  nerves,  I,  70;  VII, 

395 
Myasthenic,  VII,  401 
Myotonic,  VII,  402 
Neurotonic,  VII,  403 
Normal,  VII,  396 
Electricity  and  the  nervous  system,  p.  29 
Electricity     in     examination     of     nervous 

patients,  I,  70-1;  VII,  395 
Embolism,    Cerebral,    X,    505;    XIV,    832; 

XVI,  1062 
Emotion,  p.  10 
Emotional  insanity,  Diseases  causing,  XVI, 

1080 
Emotions,  Disturbances  of,   I,   1;   III,  204 

Tests  for,  I,  7 
Emprosthotonus,   IV,   265 ;   XI,   590,   606 
Encephalitis,  Acute  multiple,  X,  495,  543-4; 

XVI,   1064 
Encephalomyelitis,  XII,  659 
Endarteritis,   cerebral,    Syphilitic,    II,    175; 
XVIII,  1207 
spinal,  Syphilitic,  II,  175;  XVIII,  121 1 
syphilitica,  II,  175;   XVIII,  1207,   1211 
End-organs,   p.   5 
Enophthalmus,  XVII,  1191 
Enteralgia,  XV,  988 
Epicritic  sensibility,  p.  6 
Epidemic   cerebro-spinal    meningitis :      See 

cerebro-spinal  meningitis 
Epigastric  reflex,  V,  310 

Tests  for,  I,  57 
Epilepsy,  I,  2;  II,  no,  126;  XI,  575;  XV, 
1027;  XVI,  1058,  1071 
Amnesia  in,  XI,  575 
Automatism  in,  XI,  575 


266 


INDEX 


Epilepsy,   Double  personality  in,   III,  209; 
XI,  575 
Glittering   scotoma   as   aura  of,   XIV, 

846 
Idiopathic,  XI,  575 
Jacksonian,    IX,    431;    XI,    587,    605; 

XXI,  1282-3,  1291 
Major  attack  of,  XI,  575;  XVI,  1058 
media,  XI,  575 
Minor     attack     of,     XI,     575;     XVI, 

1058 
Nocturnal,  XI,  575 ;  XVI,  1058 
Procursive,  XI,  575 
Psychic  equivalent  in,  XI,  575 
Rotatory,  XI,  575 
Spinal,  I,  60-1;  IX,  443;  X,  509,  520; 

XIV,   838 
Symptomatic,    XI,   576-96 
Epileptic  aura,  IX,  430;  XIV,  846 
cry,  XI,  575;  XVI,  1058 
dementia,    XI,    575;    XVI,    1058,    1102 
idiocy,  XVI,  1083 
insanity,  XI,  575;  XVI,  1058 
state,  XVI,  1058 
vertigo,  XV,  1027 
Epileptiform  convulsion,  XI,  571 
Erb's    juvenile     form    of     muscular    dys- 
trophy,   X,   499;    XIII,   786;    XVII, 
1151 
paralysis,  IX,  454;  X,  490 
sign,  IX,  452;  XI,  614 
syphilitic     lateral     sclerosis,     X,     525; 
XVIII,   1212 
Erotic  excitement  in  dementia,  XVI,  1105 
Erroneous  personality,  III,  209 
Eruptions,     cutaneous,     Diseases     causing, 

XVII,  H34 
Erythromelalgia,  XV,   1010;   XVII,   1 198 
Erythropsia,  XIV,  843 
Essential  tremor,  XII,  681 
Ethics,  p.   13 

Etiology  of   nervous  diseases,  I,   1;   II,  83 
Eulenberg's  disease,  IV,  265;   XI,  613 
Eunuchismus.     Pituitary,  XXI,  1279 
Examination  of  patients,  I 
Excessive   sweating,  XVII,    1203 
Excitability.      Nervous,  p.  5 
Excitation,   Maniacal,   XVI,   1115 
Exhaustion    in    etiology    of    nervous    dis- 
eases, II,  95;  XIII,  757 
Vertigo  from,  XV,  1022 
Exophthalmic  goitre,   I,  20;   II,   131;  XII, 

672;   XVII,  1 193 
Extension   of   inflammation  in  etiology  of 

nervous  diseases,  II,  96 
External  capsule,  Symptoms  of  lesions  of 

the,  XXI,  u;3 
External    rectus.    Paralysis    of    the,    XIV, 
870 


Eye  as  cause  of  headache,  The,  XV,  943, 
952 
in  disease,  I,  24 
Eyeball,  Conjugate  deviation  of  the,  XIV, 
817 
Displacement  of  the,  XIV,  877 
Limitation  of  motion  of  the,  XIV,  816 
Optic  atrophy  in  diseases  of  the,  XIV, 

914 
Paralysis    of    external    rectus    of    the, 
XIV,  870 
of   inferior  oblique   of    the,   XIV, 

875 

rectus  of  the,  XIV,  873 
internal    rectus    of    the,    XIV, 
871 
muscles  of  the,  XIV,  816 
superior  oblique  of  the,  XIV,  874 
rectus  of  the,  XIV,  872 
Spasm  of  muscles  of  the,  XIV,  876 

Face    center,    Symptoms    of    lesions    of; 

XXII,  1380,  1381   1383 
Facial  expression  in  disease,  I,  20 
diplegia,  XII,  703 
hemiatrophy,  XVII,  11 79 
hemihypertrophy,  XVII,  1 180 
monoplegia,  XII,  703 
nerve,     Localization     of     lesions     of, 

XXII,  1317 
nucleus,  Symptoms  of  lesions  of,  XXII, 

1329-31 
paralysis,   XII,   703;   XIII,  751 1  XIV, 

928;  XXII,  1329-36 
spasm,  or  cramp,  XII,  726 
Facio-scapulo-humeral    type    of    muscular 

dystrophy,  X,  497 
False  image.  Position  of,  XIV,  816 
Family  gangrene,  XVII,  1 196 
history,  I,  2 

myoclonus  epilepticus,  XI,  604 
periodic  paralysis,  X,  555 
Faradic  excitation  of  nerves  and  muscles, 

I,  70-2;  VII,  395 
Faradism     in     examination     of      nervous 

patients,   I,  70-2;  VII,  395 
Fatty  tissue,  atrophy  of,  Diseases  causing, 
XVII,   1136 
hypertrophy   of,   Diseases   causing, 

XVII,   1137 
trophic   lesions  of,   Diseases  caus- 
ing, XVII,   HJ-t 
Fear,   111. 

Feeble-minded,  i>    [9;  XVI,  1092 
Febrile  or   toxic   convulsion,    XI,    595 
Fcstinating    gait     (Festinationl,    XI,    612; 

XII.  677;   Mil,  ;«),  800 
Fibrillar]  (Fibrillation),  IV, 

292 
Diseases  causing.  XII.  641 


267 


INDEX 


Field    of    vision,    Limitation    of    the,    IX, 
425 
Diseases  causing,  XIV,  815 
Tests  for,  I,  14 
Fits,  I,  1 :     See  also  convulsion  and  spasm 
Flaccid  paralysis,  IV,  252 

Diseases  causing,  X,  472 
Tests  for,  I,  39 
Foot  drop,  I,  21 ;  X,  488,  404;  XIII,  788 
Formication,  VI,  375 

Formula  of  electrical  reaction  of  degenera- 
tion, VII,  399 
of  normal  electrical  reaction,  VII,  396 
Foul  air  headache,  XV,  954 
Fourth    ventricle,    lesion    within,    Vertigo 

from,  XV,  1018 
Foville's   paralysis,   XXI,    1269 
Fragility  of  bone,  XVII,  1185 
Free-will,  pp.  23-4 
Frenzy,  Maniacal,  XVI,  1115 
Friedreich's  hereditary  ataxia,  II,  104,  123; 
XII,  652,  670,  687 ;  XIII,  762,  781 
paramyoclonus  multiplex,  XI,  603 
Frontal  convolution   (inferior),  Symptoms 
of  lesions  of  the,  XXII,  1390 
(middle),  Symptoms  of  lesions  of 
the,  XXII,  1389,  1399 
headache,  XV,  952 

lobes,    Symptoms    of    lesions    of    the, 
XIV,  885 ;  XXI,  1282 

Gait,  ataxic,  Diseases  causing,  XIII,  740 
in  disease,  I,  21 ;  XIII,  736 
disorder    of,    Diseases    causing,    XIII, 

736 
Festinating,  XII,  677;  XIII,  766,  800 
High-stepping,  X,  488;  XIII,  787-9 
Mowing,  XIII,  794 
Paralytic  and  flaccid,  XIII,  741 

and  spastic,  XIII,  742 
Scissors,   XIII,  742 
Galton's  whistle,  I,  15 
Galvanic  excitation  of  nerves  and  muscles, 

VII,  395 
Galvanism     in     examination     of     nervous 

patients,  I,  71 
Ganglionic     disorders,     Diseases     causing, 

XVII,  1 128 
Gangrene,  Family,   XVII,   1196 

Symmetrical,  XV,  ion;  XVII,  1195 
Gastralgia,  XV,  986 
Gastric  crises,  IX,  433 
General  appearance  in  disease,  I,  20 
General  paresis :    See  paresis 

sensation,  p.  8 
Geniculate  bodies,   Lesions  of,   XIV,  858; 

XXII,  1321 
Genital  neuralgia,  XV,  990 
Gerlier's  vertigo,  XV,  1031 
Gigantism,  XVII,  1 183 


Girdle  pain,  VI,  374 

Diseases  causing,  XV,  935 
Glaucoma,  XIV,  864;  XV,  943 
Glioma,  II,  124 

Central,  X,  552 
Glittering  scotomata,  XIV,  846 
Globus  hystericus,  IX,  426;  XI,  586;  XVI, 

1074 
Glosso-pharyngeal   spasm,   or  cramp,   XII, 

727 
Glossy  skin,  I,  40;  XVII,  1160 
Glove  form  of  anesthesia,  VI,  345 ;  IX,  425 
Gluteal  paralysis,  XII,  719 
reflex,  V,  307 

Tests  for,  I,  57 
Gordon's  reflex,  V,  305 
Graefe's  symptom,  XII,  672;  XVII,  1 192-3 
Grandeur,  Delusion  of,  XVI,  1 1 13 
Grand  mal  (le),  XI,  575;  XVI,  1058 
Grasset  and  Gaussel's  phenomenon,  IX,  458 
Gratiolet,  Lesion  of  the  optic  fasciculus  of, 

XIV,  855-6;   XXII,   1364 
Grave's  disease,  XII,  672;  XVII,  1193 
Green  vision,  XIV,  844 
Gumma,  II,  172 

Isolated,  cerebral,  XVIII,  1206 
spinal,  XVIII,  1210 
Gustation.     Cortical  center  of,  p.  7 
Gustatory  sensations,  p.  7 

Habit,  p.   16 

chorea,  IV,  274;  XI,  626 

spasm,  XI,  626 
Habitation  in  nervous  diseases,  I,  2;  II,  89 
Habitual  criminals,  XVI,  1094 
Hallucinations,  p.  19;  I,  4,  20;  III,  213 
Hallucinatory    insanity,    Diseases    causing, 

XVI,  1078 
Hallucinosis,  Alcoholic,  XVI,  1109 
Hand,  Ape's,  XII,  714 

Claw,   X,  547;   XII,  715 

Obstetrical,  XI,  614 

Trident  shaped,  XVII,   1177 
Haphalgesia,  VI,  380 
Hare's  eye,  XII,  703 
Head  in  disease,  The,  I,  22;  XVI,  1076 
Head's  researches  on  sensibility,  p.   16 
Headache,  I,  I ;  XV,  934 

Alcoholic,  XV,  953 

Anemic,  XV,  952,  958 

Aural,  XV,  952 

in  cerebral  abscess,  XV,  960,  965 

Congestive,  XV,  957 

Constipation,  XV,  952,  955 

Diseases  causing,  XV,  934 

Dyspeptic,  XV,  952 

Foul  air,  XV,  954 

Frontal   in  disease,  XV,  952 

High   blood  tension  causing,   XV,  957 


268 


INDEX 


Headache,   Hydrocephalic,   XV,  960 

Indurative,  XV,  962 

Infection,  XV,  963 

Meningitic,  XV,  961,  964 

Menstrual,  XV,  949 

Migraine,  XIV,  836,  854;  XV,  949,  1028 

Morphine,  XV,  953 

Neurasthenic,  XV,  959 

Occipital,  XV,  952 

Ocular,  XV,  952 

Pachymeningitis  XV,  961 

Pelvic,  XV,  952 

Rheumatic,  XV,  962 

Sinus  thrombosis  causing,  XV,  964 

Sunstroke  causing,  XV,  966 

Temporal,  in  disease,  XV,  952 

Toxic,  XV,  963 

Tumor  causing,  XV,  960 

Uremic,  XV,  956 

Vertex,  in  disease,  XV,  952 
Heatstroke  or  sunstroke,  XI,  589;  XV,  966; 

XVI,  1068 
Hearing,   p.  8 

Cortical   center  of,  p.  8 

Diseases    causing    disorders    of,   XIV, 
808 

Loss  of,  XIV,  820 

Tests  for,  I,  15 
Hebephrenia,  XVI,   1097 
Heine-Medin's   disease,  X,  495 
Hematorrhachis,  X,  524;  XV,  973 
Hemeralopia,  VI,  360 
Hemianesthesia,   alternans  or  crossed,  VI, 
345;  XXI,  1269 

dolorosa,  XXI,  1275 

and  hemianalgesia,  VI,  345;   IX,  425; 

XXI,  1268-70 

Hysterical,  VI,  345 ;  IX,  425  ;  XIV,  834 
Transference  of,  IX,  425;  XIV,  834 
Hemianopia,  VI,  362;  XIV,  815,  800 

Bi-temporal,   VI,  362;   XIV,  815,  860, 
892;  XXII,  1319 
Diseases  causing,  XIV,  815 
Homonymous,  VI,  362;  XIV,  815,  800; 
XXI,    1285;    XXII,    1342 
Diseases  causing,  XIV,  815 
Horizontal,  XIV.  862 
Localization  of,  XXI,  1275,  1283,  1285; 

XXII,  1315.   J342-3 

Nasal,  VI,  362;  XIV,  815;  XXII,  1320 

Diseases  causing,  XIV,  815 
Quadrantic.   VI.  363;   XIV,  815;   XX, 

U85;  XXII.  1343 
Tests  for,  I,  14 
Hemiataxin.   XII.  654-7 
Hemiatrophy,    Facial,    XVII,    ii;j 
Hemicrania.  XV,  >>vi 

angio-paralytica,  XV,  949 
iii',1,  XV,  tj.|'> 
borea,  IV,  27a .  X,  5x0;  XI.  573 


Hemichromatopsia,  VI,  364;   XIV,  847 
Hemihypertrophy,   Facial,   XVII,   1180 
Hemiopic  pupillary  reflex,  V,  334 

Diseases  causing,  XIV,  890 
Tests  for,  I,  26 
Hemiplegia,  I,  21;  IV,  254;  X,  478-9 

alternans,    IV,    256;    X,    537-42;    XV, 
1017;  XXI,  1268 
Facial,  IV,  256;  XXI,  1269 
Hypoglossal,   IV,  256;   XXI,    1268 
Oculo-motor,   IV,  256;   XXI,   1270 
Angio-spastic,  X,  554 
Complete,  IV,  254;  XXI,  1276 
Crossed :     See  H.  alternans 
Diseases  causing,  X,  478-9 
Hysterical,  XIII,  793 
Infantile :    See  cerebral  palsy  of  child- 
hood 
Lacunar,  XVI,  1063 
Organic,  XIII,  794 
Partial,  IV,  254 

Spinal,   IX,  442;   X,   509;   XIV,  838; 

XV,  981 

Hemorrhage  in  brain   stem,   X,   535;  XII, 

656 

Cerebral,   II,    146;    X,   503;    XI,   588; 

XIV,  832,  857;  XVI,  1043,  1061 

cerebro-spinal  fluid  in,  VIII,  41 1-3; 

XIX,  1240 
into  ventricles,  X,  504 
internal,  Coma  in,  XVI,  1056 

Vertigo  in,  XV,   1023 
Meningeal,  cerebral,  II,   146;   X,  502; 
XVI,   1060 
Cerebro-spinal    fluid   in,   VIII, 
41 1-3;    XIX.    1240 
Spinal,  II,  146;  X,  524 

Cerebro-spinal    fluid   in,   VIII, 
41 1-3;  XIX,  1230-40 
or  injury  of  spinal  cord,  above  cervical 
enlargement.  X.  51a 
in  cervical  enlargement.  X.  548 
dorsal  region,  X,  516 
lumbar  region,  X,  4S4 
or  softening  in  cms  cerebri,   X,  537 
in  medulla.  X,  541 
pons,  X,  539 
Hepatic  crises,  IX,  433 
Hereditary  ataxia,  II,  104.  123;  XII,  651-2, 
"■)  ;■•,  usr:  xiii.  76a,  781-3 
chorea:     See  chorea 
1 1  iniiity  in    nervotu    diseases,    l.    a;    II, 

81 
Herpes,  I,  40;  XI,  ggo;  X  r. 
Herpes  zoster,  XVII.   1166;   XIX.    1234 
Cerebro-spinal  fluid  in,  XIX.   1934 
Herpetic  neuritis,  XV,  940,  978 

li,  XII,   73] 
High  stepping  gait,  X,  4SN;  Xll.  710;  XIII. 
741 


269 


INDEX 


High   tension  headache,   XV,   957 

vertigo,  XV,  1025a 
Hip.       Congenital     dislocation     of,     XIII, 

786a 
Hippus,  V,  336 
History  taking,  I,  1 

Homonymous     hemianopia:       See     hemi- 
anopia 

Scotomata,  XIV,  863 
Hunger,  p.  8 
Huntington's    hereditary    chorea,    II,    103; 

XI,  623 
Hydrocephalic  cry,  XI,  593 

idiocy,  XVI,  1082 
Hydrocephalus,  I,  22;  II,   119 

Cerebro-spinal     fluid    in,     VIII,    411; 
XIX,  1238 

Headache  in,  XV,  960 

Optic  neuritis  in  XIV,  905 
Hydrophobia,  II,  171 ;  XI,  607 
Hydrorrhoea   nasalis,    XXI,    1279 
Hypakusia,  VI,  355;  XIV,  820 
Hypalgesia,  VI,  349;   XIV,  810 
Hyperakusia,  VI,  372;  XIV,  820 
Hyperalgesia,  VI,  367 

Tests  for,  I,  50 

Thermic,  VI,  366 
Hyperemic  reflex,  V,  326 
Hyperesthesia,  VI,  366;   XIV,  813 

Tests  for,  I,  48 

Thermic,   VI,   368 
Hypergeusia,  VI,  370 
Hyperhidrosis,  XVII,   1203 
Hyperkinesis,  IV,  242 
Hyperosmia,  VI,  369 
Hyperostosis  cranii,  XVII,  1181 
Hypertonia,  I,  39;  IV,  240;  X,  473 
Hypertonic  paralysis,  IV,  251 ;  X,  473 
Hypertrophic       pulmonary       osteo-arthro- 

pathy,  XVII,   1184 
Hypertrophies,  Localized,  XVII,  1188 
Hypertrophy    of    bone,    Diseases    causing, 
XVII,  1139 

of  fat.  Diseases  causing,  XVII,  1 137 
muscle,  I,  40 

Diseases   causing,   XVII,   1131 
in  an  athlete,  XVII,  1154 
skin,  Diseases  causing,  XVII,  1 133 
Hypesthesia,  VI,  348;  XIV,  810 
Hypnotism,  XVI,  1069 
Hypochondriasis,  III,  216;  XVI,  1073 
Hypogeusia,  VI,  357;  XIV,  809 
Hypoglossus  paralysis,  XII,  706;  XIII,  752 

spasm  or  cramp,  XII,  729 
Hypokinesis,  IV,  241 
Hyposmia,  VI,  356 

Hypotonia,  I,  39;  IV,  240;  X,  472,  483 
Hypotonic  paralysis,  IV,  252;  X,  472 


Hysteria,  I,  2;  II,  ill,  128,  130,  153,  179; 
XIV,  843,  848,  866,  926;  XV,  950, 
971 ;  XVI,  1070,  1074 

Concentric  limitation  of  field  of  vision 
in,  IX,  425;  XIV,  866 

Perversion  of  vision  in,  XIV,  843,  848 

Traumatic,  XVI,  1075 

Vertigo  from,  XV,  1033 
Hysterical  amblyopia,  XIV,  851a. 

anesthesia,    p.    7;    VI,    345;    IX,    425; 
XIV,  834 
Tests  for,  I,  48 

aphonia,  XIII,  748,  759 

ataxia,  XII,  664 

backache,  XV,  971 

chorea,  XI,  628 

coma,  XVI,  1069 

contracture,  X,  618 

convulsion,  XI,  586 

deafness,  XIV,  924 

diplopia,  XIV,  878 

hemianesthesia,  IX,  425 ;  XIV,  834 

hemiplegia,  XIII,  793 

hyperakusia  and  parakusia,   XIV,   926 

joint    XV,  1000 

mutism,  XIII,  747 

neuralgia,  XV,  950 

paralysis,    X,    527;    XIII,    747-8,    759, 
793;  XIV,  878;  XVI,  1074 

spasm,  X,  618 

symptoms,  IX,  425 

tremor,  XII,  674 
Hystero-epilepsy,  XI,  586 
Hysterofrenic   areas,   IX,  428 
Hysterogenic  areas,   IX,  427 

Ictus,  X,  479 

laryngcus,  IX,  433 
Ideas,  pp.  10,  13 
Idiocy,   p.   18;    II,    101;    XIII,   743!    XVI, 

1081 
Idioglossia,  XIII,  750 

Idiopathic  epilepsy,  XI,  575;  XVI,  1058, 
1071 

idiocy,  XVI,  1081 

imbecility,  XVI,  1091 

muscular  dystrophy,  IX,  498 

neuralgia,   XV,   937 
Idiots  savants,   XVI,   1089 
Illuminating  gas  poisoning,   XVI,   1055 
Illusions,   p.   19;   III,  214 
Imagination,  p.   14 
Imbecility,  p.  18;  II,  101 ;  XVI,  1088,  1091 

moral,  XVI,  1094 
Immobile  eyeball,  X,  545 

pupil,  V,  333;  X,  545 
Indurative  headache,  XV,  962 
Infantile  diplegia,  X,  501 

hemiplegia,  X,  501;  XI,  577,  630;  XIII, 
798;   XVI,  1048 

paralysis :     See   poliomyelitis 


270 


INDEX 


Infantilism,  XVI,   1093 
Infectious  chorea,  XI,  622 
headache,  XV,  963 
nervous  diseases,  I,  I,  II,  93 
Inferior  oblique  muscle,  Paralysis  of,  XIV, 
875 
rectus  muscle,  Paralysis  of,  XIV,  873 
Inflammation  of  brain  stem,  X,  535;  XII, 
656 
Cerebral :     See  meningitis  and  abscess 
of  nerves  :     See  neuritis 
spinal  cord :     See  spinal 
Infra-maxillary  neuralgia  or  neuritis,  XV, 
94S 
orbital  neuralgia  or  neuritis,  XV,  944 
Ingravescent  apoplexy,  XVI,   1060-3 
Inherited  nervous  diseases,  II,  84 

tendencies,  II,  85 
Inhibition,  p.  22 
Injury,  I,  1;  II,  135 
Injury  of  cauda  equina,  X,  487 
brachial  plexus,  X,  490 
nerve,  X,  489,  492;  XIV,  822;  XVII, 

1 146 
optic  nerve,  XIV,  904 
or  hemorrhage  of  spinal  cord,  cervical 
enlargement,  X,  548 
cervical  region,  X,  512 
dorsal  region,  X,  516 
lumbar  region,  X,  484 
spinal  cord,  XIV,  838 
Innervation   feelings  and  memories,  p.  12; 

III,  221 
Insanity,    p.    18;    I,   2;    II,    109,    129,    154; 
XVI,   1041 
Adolescent  or  juvenile,  XVI,  1096 
Catatonic,  XVI,  1098 
Circular,   XVI,   1 116 
Confusional,  XVI,  1106 
Delusional,  XIII,  746;  XVI,  1079 
Emotional,  Diseases  causing,  XVI,  1080 
Epileptic,  XI,  575 ;   XVI,  1058 
hallucinatory,   Diseases   causing,   XVI, 

1078 
Hebephrenic,  XVI,  1097 
Maniacal  depressive,  XVI,   11 17 
Paranoid,  XVI,   1099 
Pott-epileptic.  XI.  575;  XVI,  1058 

febrile,  XVI,  1107a 
Recurrent,   XVI,   1 117 
Septic,  XVI,   1107a 
Tests   fur,  I,  4 

\VI,   1107a 
Insolation,  XI.  589;  XV.  966;  XVI,  1068 
Insomnia,  I,  18 
Inspection  in  diagnosis,  I. 
Insufficiency  of  ocular  muscles,  XII,  692 
Intelligence,  p.  17 

1  titturbancei  "f,  lit,  202 
Tests  for,  I,  5 


Intention  tremor,  IV,  290;  XII,  645 

Diseases  causing,  XII,  643 
Intercostal  neuralgia,  XV,  977 
spasm  or  cramp,  XII,  732 
Interlacing  of  color  fields,  I,  14;  XIV,  849 
Intermittent    limping    or    claudication,    X, 
5541  XVII,  1199 
paralysis,   X,  471 
Internal  capsule, 

Symptoms  of  lesions  of  the,  XIV, 
857;    XXI,    1276;    XXII,    1354, 
1361,  1385 
rectus  muscle,   Paralysis  of,  XIV,  871 
sensations,   pp.  8,   10 
Interscapular  reflex,   V,   311 

Tests  for,  I,  57 
Intoxication,     Alcoholic,     XII,     658,    663; 

XIII,  764,  780 
Inversion  of  color  fields,  I,  14;  XIV,  849 
Iridoplegia,  V,  339 
Iritis,  I,  24 
Irritation  of  sympathetic  ganglia,  Diseases 

causing,  XVII,  1143 
Ischemic  reflex,  V,  325 
Island  of   Reil,   Symptoms  of   lesions  of, 
XXI,  1278 

Jacksonian  epilepsy,  IX,  431 ;  XI,  587,  605 
Location  of  lesions  causing,  XXI, 
1282-3;  XXII,  1291 
Jargon  speech,  III,  225;  XIII,  775 
Jaundice,  Yellow  vision  in,  XIV,  842 
Jaw  reflex,  V,  322 

Tests  for,  I,  65 
Jendrassik's   method   of   reflex    reinforce- 
ment, I,  68 
Joints,  trophic  lesions  of,  Diseases  causing, 

XVII,  1 126 
Joy,  III,  236 
Juvenile  insanity,  XVI,   1096 

Kahler's  disease,   XVIII   1209 
Kak-ke  :     See  neuritis,  multiple 
Kalmuck  idiots,  XVI,   1093 
Keratitis,  I,  24 
Kernig's  sign,  V,  319 

Tests  for,  I,  66 
Kinesthetic   memories,   pp.    1.,   97 
Knee-clonus,  I,  61 
Knee-jerk,  V,  318 

Tests  for,  I,  61 
Knowledge,  Tests  for  general,  I.  5 
Klumpke's  paralysis,   IX,  455;  X,  490 
Korsakow*s  psychosis,   X,  488;   XVI,   1100 
Kyphosis,  I,  83;  XVII,  It 83 

Labyrinth  disease,  XIV,  918 
Labyrinthine   vertigo,  XII,  685 
Labio-glosso-pharyngeal   pvalytit,  X,  546 
Lacunar  htjnlplegia,   XVI,  1063 


271 


INDEX 


Lagophthalmus,  XII,  703 

Lalling,  XIII,  750 

Landouzy-Dejerine      type      of      muscular 

atrophy,  X,  497,  XVII,  1151 
Landry's  paralysis,  II,   168;  X,  482 
Language,   Zone  of,  6.  28 
Laryngeal  crises,  IX,  433 
exhaustion,   XIII,   758 
nerve,  Paralysis  of  superior,  XIII,  754 
vertigo,  IX,  433 
Laryngismus   stridulus,  XI,  617;  XII,  728 
Laryngitis,  XIII,  757 
Laryngoscopy  in   examination   of   nervous 

patients,  I,  77 
Larynx,  Anesthesia  of,  XIII,  754,  760,  761 
Lasegue's  symptom,  IX,  429 
Lateral  column :     See  spinal  cord 
sclerosis,   X,  525;   XIII,   797 

Amyotrophic.    X,    547;    XII,    695; 

XVII,   1 149 
Erb's  syphilitic,  X,  525 
Lateropulsion,  XXI,  1269,  1272-3 
Lead  colic,  II,  158;  XV,  988 
convulsion,  XI,  576,  584 
palsy,  II,  158;  X,  494;  XIII,  788;  XVI, 

1050 
poisoning,  Optic  neuritis  in,  XIV,  901 
Leg  center:     See  localization 
Le  grand  mal  of  epilepsy,  XI,  575;  XVI, 

1058 
La  petit  mal  of  epilepsy,  XI,  575 ;  XVI,  1058 
Lemniscus,   Lesions   of,    causing   deafness, 

XIV,  922 
Leontiasis  ossea,  XVII,  1181 
Leprous  neuritis,  II,  140;  XVII,   1169 
Lethargy,  African,  II,  141 
Leucoderma,  XVII,  1162 
Levator  palati,  Paralysis  of,  XIII,  753 
Limping,  Intermittent,  X,  554;  XVII,  1 199 
Lisping,  XIII,  750 
Little's  disease,  X,  501 
Local  asphyxia,  XVII,  1195 
cyanosis,  XVII,  1195 
paralysis,  IV,  259;  XII,  636 
spasms,  XII,  637 
syncope,  XVII,  1195 
Localization,  p.   12;  XX,  XXI,  XXII 
at  base  of  cranium,  XXI,  1274 
by  Jacksonian  epilepsy,  XXII,  1291 
by  paralysis,  motor  and  sensory,  XXII, 

1290 
cerebellar,  XXI,  1272 
vermis,  XI,  610 
Direct,  tract,  XII,  654 
hemispheres,  XI,  609 
peduncle  (middle),  XXI,  1273 
Cerebral : 

brain  stem,  X,  535-46;  XII,  656; 
XIV.  830;  XXI,  1268-71; 
XXII,  1375,  1378,  1398 


Localization,    cerebral,    abducens    nucleus, 
XIV,  882;  XXII,   1328 
corpora     quadrigemina,     XXI, 

1271 
crura  cerebri,   X,   537-8;   XII, 
676;     XXI,      1270;     XXII, 
1324-29.   1384,  1398 
dysarthria       and       dysphagia, 
XXII,     1375,     1378,     1382-3, 
1388 
facial  nucleus,  XXII,   1329-31 
fourth  ventricle,  XV,  1018 
ganglia  at  base,  XXI,   1268-80 
lemniscus,   XIV,  922 
medulla   oblongata,   X,   541-2; 

XXI,  1268;     XXII,     1375, 
1382,  1388,  1398 

motor    cranial    nuclei,    XXII, 

1304 
pons  Varolii,  X,  539-4° ;  XIV, 

884;      XXI,      1269;     XXII, 

1328-31,     1353,     1383,     1388, 

1398 
ponto-cerebellar    angle,    XXII, 

1363 
red  nucleus,  XXII,  1325 
rubro-spinal    tract,    XII,    676; 

XXII,  1325 

sensory   cranial   nuclei,   XXII, 

1302 
sixth    cranial    nucleus,    XXII, 

1327 
third    cranial    nucleus,    XXII, 
1323,    1326 
hemispheres : 

agraphia,    XXI,    1282;    XXII, 

1389 
alexia,  XXII,  1391 
angular  gyrus  of,  XXII,  1391 
aphasia,    motor,     XXI,     1282; 
XXII,  1390 
sensory,  XXI,  1284;  XXII, 
1368 
arm  center,  XXII,   1349,   1352, 
1369,   1376,   1379.   1381,  1387, 
1401 
astereognosis,      XXII,       1346, 

1369 
blindness,  Psychic,  XXI,  1285; 

XXII,  1344,   1367 
calcarine  fissure,  XXII,  1364-6 
central    convolution,    anterior, 
XXII,     1373.     1376, 
1379-81,  1387,  1400-5 
posterior,  XXII,  1348-9. 
1352,  1369 
claustrum,   XXI,   1278 
corpus  callosum,   XXI,   1277 
corpus    striatum,    XXI,    1276; 
XXII,  1386 


272 


INDEX 


Localization  in   cerebral  hemispheres: 
cortical   lesions,  XXI,   1286 
external  capsule,  XXI,  1278 
face-center,   XXII,  1380-3 
facial  fibers,  XXII,  1317 
frontal    convolution,    inferior, 
XXII,  1390 
middle,     XXII,     1389, 
1399 
frontal  lobe,  XIV,  885;  XXI, 

1282;  XXII,  1389-90 
geniculate   bodies,  XXII,   1321 

ganglion,  XXII,  1333-4 
hemianopia,  homonymous, 

XXII,  1342-3 
internal     capsule,     XIV,    857; 
XXI,      1276;     XXII,     1354, 
1361,  1385 
Island  of  Re:l,  XXI,  1278 
leg   center,   XXII,    1348,    1352, 
1355,   1362,   1373,   1379,   1387, 
1402 
nucleus  caudatus,  XXI,   1276 
nucleus  lenticularis,  XXI,  1276 
occipital     lobe,     XIV,     850-6; 

XXI,  1285;  XXII,  1367 
optic    fasciculus    of    Gratiolet, 

XIV,  855-6;  XXII,  1364 
optic    thalamus,     XXI,     1275; 

XXII,  1386 

parietal  lobe,   XII,  657;  XXI, 
1283;  XXII,  1403-5 
lobule     (inferior).    XXII, 
1362 
(superior),  XXII,  1355 
pineal  gland,  XXI,  1280 
pituitary  gland,  XXI,  1279 
Reil,  Island  of,  XXI,  1278 
temporal   convolution    (superi- 
or), XIV,  925;   XXI,   1284; 
XXII.  1368 
cranium,  At  base  of,  XXI,  1274 
Failure  of,  VI,  376 
neurons,   Central,   XXII,   1293 

Peripheral,  XXII,  1292 
Peripheral : 

brachial  plexus.  XXII,   1306 
cauda  equina,   XXII.   1308 
chorda  tympani,  XXII,   1335-6 
cranial  motor  nerves,   XXII,   1303 

sensory  nerves,    XXII,    1301 
facial  nerve.  XXII,  i,u;,  1332-6 
hemianopia,  XXII,  131 
lumbar  plexus,  XXII.  1306 
ocular  muscles,  XXII,  1316 
optic  chiasm,  XIV,  851,  860-1,  892; 
XXII,    13.0-20 
nerve,  XIV,  BSI;   XXII,   1318 

tract  XIV,  858-9,  893;  XXII, 

I.U'I 


Localization,  peripheral,  orbit,  XXII,  1322 
sixth  cranial  nerve,   XXII,   1327 
spinal  nerves,  XXII,  1303-8 
third  cranial  nerve,  XXII,  1323 
sensation  tests  for,  I,  53 
Spina!  cord : 

anterior  commissure,  XXII,  1357-9 
horn,  XXII,  1304 
nerve  roots,   XXII,   1304 
Burdach's  column,  XXII,  1302 
central  gray  matter,  XXII,  1357-9 
cervical    enlargement    and    region, 
XXII,  1310,  1350-1,  1358-9,  1374, 
'377,  1397 
direct  cerebellar  tract,  XII,  654 
dorsal   region,   XXII,    1347,    1356, 

1372,  1395 
lateral  column,  XXII,    1356,   1358, 

1360,    1372-74,   1377.    1396 
lumbar   enlargement,    XXII,    1309, 

1357 
posterior     column,     XXII,      1347, 
I350-I,   1396 
horn,  XXII,  1302 
nerve  roots,  XXII,   1302 
Segments : 
cervical ; 

8th,  XX,  1263 
7th,  XX,  1264 
6th,  XX,  1265 
5th,  XX,  1266 
4th  to  1st,  XX,  1267 
dorsal ; 

12th,  to  3rd,  XX,  1260 
2nd,  XX,  1261 
1st,  XX,  1262 
lumbar ; 

5th,  XX,  1255 
4th,  XX,  1256 
3rd,  XX,  1257 
2nd,  XX,  1258 
1st,  XX,  1259 
sacral ; 

5th,  XX,  1250 
4th,  XX,  1251 
3rd.  XX.  iasa 
and,  XX,  1253 
1st,  XX,  [354 
vision,  Disturbances  of,  XXII.  1315 
Localized     atrophies     and     hvpertrophies, 

XVII,  :  188 
Lockjaw:    See  tetanus 
Locomotor  ataxia:     Sec  I 
Long  thoracic  nerve,   r.ir.ilv  -i~  of.  XII,  709 
Lumbar  enlargement:     See  ipinal 

plexus,   spasm   or   cramp  of,   XII,   733 
symptoms,    of    lesions    of,     XXII. 
tJOO 
puncture,    I,   74,    XI,  590 

■    of,  I.  n 


INDEX 


Lumbo-abdominal  neuralgia,  XV,  989 
Lyssa,  XI,  607 

Macrocephalia,  I,  22 

Macropsia,  VI,  387 

Major  attack  of   epilepsy,  XI,   575;   XVI, 

1058 
Mania,  III,  236 

Acute  alcoholic,  XVI,  1 109 
Epileptic,  XI,  575 
Primary,  XVI,  11 15 
Symptomatic,    or    Delusional,   or   Sec- 
ondary,  XVI,   mi 
Maniacal   excitation,   XVI,    n  15 
depressive  insanity,  XVI,  1117 
fre.izy,   XVI,    HIS 
Marie-Tooth-Charcot's    type    of    muscular 

atrophy,  X,  496 
Marie's  hereditary  cerebellar   ataxia,  XII, 
651,  669-70;  XIII,  782 
idea  of  aphasia,  XIII,  739 
Mask-like  face,  XI,  612;   XII,  677;  XIII, 

766,  800 
Mastodynia,  XV,  982 
Masturbation  in  nervous  diseases,  I,  2 
Maxillary  reflex,  V,  322 
Mechanical     irritability     of     nerves     and 

muscles,  I,  67 
Median  paralysis,  XII,  714 
Medulla    oblongata,    Hemorrhage    in    or 
softening  of,   X,  541 
Localizing  symptoms  :     See  localization 
Tumor  of,  X,  542 
Meig's  disease,  XVII,  1202 
Melancholia,  III,  234 
agitata,  XVI,  1 1 12 
attonita,  XVI,  11 12 
cum  stupore,  XVI,  1 1 12 
Primary,  XVI,   n  14 
raptus,  XVI,  1112 

Secondary  or   Sympathetic,  or   Symp- 
tomatic, or  Delusional,  XVI,  1112 
Memories,  Innervation,  III,  221 
Memory,  p.   II 

Disturbances  of,   I,   1 ;   III,  203 
Tests  for  defects  in,  I,  6 
Mendel-Bechterew's     reflex:     See     dorsal 

foot  reflex 
Meniere's    disease,    XII,    650,    685;    XIV, 
918;  XV,  1019 
Deafness  in,  XIV,  918 
Vertigo  in,  XV,  1019 
Meningeal  apoplexy,  II,  146;  X,  502,  524; 

XI,  588;  XVI.  1060 
Meningismus,   XI,  594 
Meningitis,  II,  118,  122,  147,  166,  183;  XI, 
590,  608;  XVI,  1045 
Cerebral,  X,  508;  XI,  590,  608;  XIV, 
831;     XV,     1032;     XVI,     1045; 
XVIII,   1208-9 
Vertigo  in,  XV,   1032 


Meningitis.    Cerebro-spinal,    XI,    591.    608; 
XVIII,  1214;  XIX,  1226-9 
fluid  in,   VIII,  410;   XIX,    1226-9, 
1239 
Gummosa,     II,     173;     XVIII,     1208-9, 

1213-4 
Headache  in,  XV,  961,  964 
Localized,  X,  508 
Optic  neuritis  in,  XIV,  906 
Purulent,  XI,  592;  XIX,  1227 

Cerebro-spinal  fluid  in,  XIX,  1227 
Serous,  XI,  594;  XIX,  1239 

Cerebro-spinal  fluid  in,  XIX,  1239 
spinal,    Acute    and    chronic,    XI,    608; 

XV,  974,   1005;  XVIII,   1213-4 
of  spinal  cord  and  nerve  roots,  XVIII, 

1213 
Syphilitic,   XV,   980a;   XVIII,   1208-9, 

1213-4 
Tuberculous,    II,    118,    122,    188;    XI, 
593;  XIX  1228-9 
Cerebro-spinal  fluid  in,  XIX,  1228-9 
Meningocele,  II,  102 

Mental  activity,  Disturbances  of,  I,  I ;  III, 
200,  XVI,  1036 
Diseases    causing    disorders    of,    XVI, 

1036 
reaction  time,  Tests  for,  I,  5 
Mentality  weakened,  XVI,   1040 
Meralgia  paresthetica,  XV,  999 
Mercurial  tremor,  II,  159;  XII,  673 
Metamorphopsia,  VI,  385 
Metastasis  in  nervous  diseases,  II,  98 
Metatarsalgia,  XV,  1003 
Microcephalia,  I,  22;  XVI,  1084 
Micropsia,  VI,  386 
Microsmia,   XVII,    1177 
Migraine,   II,   114;   XV,  949 

Glittering  scotoma  in,  XIV,  846 
Hemianopia  in,  XIV,  854 
Vertigo  from,  XV,  1028 
Millard-Gubber's  syndrome,  IX,  439;  XXI, 

1269 
Milroy's  disease,  XVII,  1202 
Mind,  p.  17 

Miner's  nystagmus,   XII,  684 
Minor   attack  of  epilepsy,   XI,   575 ;   XVI, 

1058,  1 07 1 
Mobile  spasm,  IV,  271 
Mongolism,  XVI,  1093 
Monocular  diplopia,  VI,  384 
Monoplegia,  IV,  258;   X,  478-9,  481 
Diseases  causing,  X,  478-9,  481 
Moral  imbecility,   XVI,   1094 

sense,  Tests  for,  I,  5 
Morphine  headache,  XV,  953 

vertigo,  XV,  1030 
Morton's  toe,  XV,   1003 
Morvan's  disease:     See  syringomyelia 


274 


INDEX 


Motion,    Diseases    causing    diminution    of, 
IV,  244;  X,  469;  XXII,  1294- 
1300 
exaggeration    of,    IV,    245-7; 

XI,  570;  XXII,  1291 
perversion   of,    IV,   243;    XII, 
635 
Disorders  of  voluntary,  IV,  240 
Motives.     Play  of,  p.  23 
Motor  aphasia,   III,   221 ;   XIII,  771 

Localization  of,  XXI,  1282;  XXII, 
1390 
ataxia,     IV,    280;     XII,    644;     XXI, 
1268-74 
Diseases  causing,  XII,  644 
impulses,  conduction  of,  p.  24 
neurons,  Diseases  of  the,  X,  469;  XI, 

570;  XII,  635-7 
oculi  paralysis,   XII,  700 
paralysis,  IV,  244;  X,  469 
Diseases  causing,  X,  469 
Localization  of,  XXII,  1290 
Tests  for,  I,  33-4 
paresis,  IV,  244;  X,  469 
points,   Electrical,   I,  70-1 ;  VII,   395 
Movements,  p.  21 
Association,  p.  22 
Autochthonous,  p.  28 
Automatic,  p.  28 
Reflex :    See  reflex 
Voluntary,  p.  22 
Mowing  gait,  XIII,  794 
Mucous  membrane  reflex  acts,  V,  298 

Tests  for,  I,  58 
Multiple  encephalitis,  Acute,  X,  495,  543-4 
neuritis:    See   neuritis 
sclerosis :    See  sclerosis 
Muscae  volitantes,  XIV,  845 
Muscle  degeneration,  IV,  252;  XVII,  1130 
-joint  sensation,  pp.  6,  8 
sense,  Loss  of,  VI,  352;  X,  488;  XII, 
661;  XIV,  812 
Tests  for  I,  42 
Diseases  causing,  XIV,  812 
tone,  I,  39;  IV,  240 
Muscles  and  nerves,  Electrical  reaction  of, 
I,  ;->;  VII,  395 
Mechanical   excitability  of,    I,  67 
trophic    lesions   of.    Diseases    causing, 
X.  47'.  7;    XVII,   1122 
Muscular  atrophy,  I,  40 

Aran-Duchenne's,  type  of,  X,  547; 

XII,  604;  XIII,  :>,:;  XVII,  1149 

Charcot-Marie-Tooth's  type  of,  X, 

496;  XII,  695 
Diseases  causing,  X,  476-7;  XVII, 

1 130 
in  chronic  paralytia,  XVII,  1 153 
Peroneal  type  of,  X,  496 


Muscular   atrophy,    Progressive   spinal,   X, 

547;  XII,  694;  XIII,  797;  XVII, 

1 149 

Spinal  or  neuritic,  X,  406;  XII,  696 

coordination,  I,  41 

dystrophies,  II,  107,  127;  X,  477;  XIII, 

786;  XVII,   1152,   1156 
dystrophy,   Erb's  juvenile,  or  scapula- 
humeral  type  of,  X,  499;  XIII,  786; 
XVII,  1 152 
in  disease,  X,  477 
Landouzy-Dejerine,  or   facio-scap- 
ulo-humeral    type    of,    X,    497; 
XIII,  786;   XVII,   1151 
Pseudo-hypertrophic    form   of,   X, 

500;  XVII,  1 156 
Simple  or  idiopathic  X,  498;  XIII, 
786,  XVII,   1 151 
hypertrophy,  I,  40 

in  athletes,  XVII,   1154 
Diseases  causing,  XVII,   1131 
insufficiency,   Ocular,   I,  24;  XII,  692; 

XIV,  816 
rigidity,    I,    31 :      See    also    paralysis 

agitans 
tonicity,  I,  39;  IV,  240 
Musculocutaneous  paralysis,  XII,  713 

-spiral  paralysis,  XII,  716 
Mutism,  Deaf,  XIII,  744 
Hysterical,    XIII,   747 
Myasthenia  gravis,  X,  553 

Tests  for,  I,  35 
Myasthenic  electrical  reaction,  VII,  401 

paralysis,  IV,  253;  X,  553 
Myatonia  congenita,  II,  105;  X,  483 
Mydriasis,  I,  24;  V,  339 
Myelitis  or 
Myelomalacia,   II,   148,   167,   184 

in  anterior  horns:     See  poliomyelitis 

cervical  enlargement,  X,  549-50;   XIV, 

835;   XVII.    ii4^a 

region,  X,  513-4;  XIV,  828 

Compression,    II,    121;    X,    520;    XIII, 

795 
Disseminated :     See  sclerosis 
in  dorsal  region,  X,  517-8;  XIV,  829 
above   lumbar   enlargement.    X.    513-4; 

XIII.  795 
in  lumbar  enlargement,  X,  485;   XIII, 

7»i;    XIV.  Xj5;    XVII,    1148a 
Multiple:    See  sclerosis 
Transverse,  XV,  980 
Myoclonia,  XII,  697 
Myoclonic  nystagmus,  XII,  691 
Myoclonus,  IV,  270;  XI,  601-4 

epileptieUi  f 
Myokymia,  IV.  .■■/.; ;  XI] 
Myopia  and  cycloplegia,  V,  331 
Myosis,    1  p;  XII,  66i;    XVII, 

iigij  XXI,  rati! 


275 


INDEX 


Myotonia,   IV,  265 

acquisita,   XI,   613 

atrophica,   XI,  613 

congenita,  II,   106;   IV,  265;   XI,  613; 
XVII,  1155 

intermittens,   XI,  613 
Myotonic  electrical  reaction,  VII,  402 
Myxedema,  I,  20;  XVII,  1163 

Nageotte's  and  Babinski's  bulbar  syndrome, 

IX,  437;  XXI,  1268 
Nanosmia,  XVII,  11 77 
Narcotism,  XV,  953;  XVI,  1054 
Nasal  hemianopia,  VI,  362;  XIV,  815 
reflex,  V,  313 

Tests  for,  I,  58 
Negativismus,  XVI,  1096-8 
Nerves  and  muscles,  Electrical  reaction  of, 
I,  72;  VII,  395 
Injury  of,   X,  489;   XIV,  822;   XVII, 

1 146 
motor  cranial,  Symptoms  of  lesions  of, 
X,  492;  XXII,  1303-7 
Facial,  XXII,  1331-6 
Sixth,  XXII,  1327 
Third,  XXII,  1323,  1326 
root,  anterior,  Symptoms  of  lesions  of, 
XXII,   1304 
posterior,  Symptoms  of  lesions  of, 
XIV,  824;  XXII,  1302 
sensory   cranial,   Symptoms  of   lesions 

of,  XXII,  1301 
spinal,    Symptoms    of    lesions    of,    X, 
489;  XIV,  822;  XXII,  1303-S-7 
Nervous  system.     Physiology  of,  p.  5 
Neuralgia,  I,  2;  II,  114,  169;  XV,  933,  937 
Achillodynia,  XV,  1001 
Angina  pectoris,  XV,  983 
Arthralgia,  XV,  1000 
Coccygodynia,  XV,  972 
Cervico-brachial,   XV,  995 
Crural,  XV,  997 
Erythromelalgia,     XV,     1010;     XVII, 

1198 
Gastralgia,  XV,  986 
Genital,  XV,  990 
Herpetic,  XV,  940,  978 
Hysterical,  XV,  950,  971 
Idiopathic,  XV,  937 
Infra-maxillary,  XV,  945 
Infra-orbital,  XV,  944 
Intercostal,  XV,  977 
Intestinal,  XV,  988 
Joint,  XV,  1000 
Lumbo-abdominal,   XV,  989 
Mastodynia,  XV,  982 
Meralgia  paresthetica,  XV,  999 
Metatarsalgia,  XV,  1003 
Neurasthenic,  XV,  959,  970 


Neuralgia,  Obturator,  XV,  998 
Occipital,  XV,  948 
Pelvic,   XV,  990 
Phrenic,  XV,  985 
Pseudo-angina  pectoris,  XV,  984 
Sciatica,  XV,  996 
Spinal,  XV,  971 
Supra-orbital,  XV,  943 
Symptomatic,  XV,  937,  952 
Syphilitic,  XV,  951 
Tabetic,  XV,  979,  987,  1004 
Talalgia,  XV,  1002 
Tic  douloureux,  XI,  602;  XV,  947 
Trigeminal,  XV,  942,  946 
Neurasthenia,   II,   113,   155,   161,   163,   178, 
180;  XV,  970;  XVI,  1072 
Perversion  of  vision  in,  XIV,  843,  845 
Neurasthenic  backache,  XV,  970 
headache,  XV,  959 
tremor,  XII,  671,  674 
vertigo,  XV,  1033 
Neuritic    or   spinal   muscular    atrophy,    X, 

496;   XII,  696 
Neuritis,  II,  142,  144.  150,  165,  185 ;  X,  489, 
492;  XIV,  822;  XV,  933.  94i;  XVII, 
1 147.  ^73 
Alcoholic,   X,  488 
Anterior  crural,  XV,  997 
Arsenical,   II,   157;   X,  488 
Brachial  plexus,  X,  490 
Compression,  XV,  939 
Crural,  XV,  997 
Diphtheritic,  X,  488 
Erythromelalgia,  XV,  1010 
Herpetic,  XV,  940,  978 
Infra-maxillary,   XV,  945 

-orbital,  XV,  944 
Leprous,  II,  140;  XVII,  1169 
Multiple,   II,    139.    160;    X,   488;    XII, 
662;  XIII,  787;  XIV,  823;  XV,  1008; 
XVII,  1 147;  XXII,  1307 
Occipital,   XV,  948 
Optic,  X,   507-8;  XIV,  897 

tract,  XIV,  859 
Simple,  XV,  941;  XVII,   1147 
Supra-orbital,  XV,  943 
Syphilitic,  II,  174;  XVIII,  1215 
Trigeminal,  XV,  942,  946 
Neuroma,  X,  491 ;  XV,  938 
Neurons,  p.  5 

Central,    Location    of    lesions    of    the, 

XXII,   1293 
Motor,  IV,  251-2;  IX,  461-2 

Diseases    of    the,   X,   469;   XVII, 
1 130 
peripheral,  Location  of  lesions  of  the, 

XXII,   1292 
Sensory,  IX,  463-4 

Diseases  of,  XIV,  804 


276 


IXDEX 


Neuroses,  II,  132  137 

Occupation,  II,  143;  XI,  616 
Traumatic,  II,  156;  XI,  616;  XII,  674; 
XV,   1033;  XVI,   1075 
Neurotonic   electrical   reaction,  VII,  403 
Nicotine  tremor,  XII,  673 

vertigo,  XV,   1030 
Nictitation,  XII,  726 
Nictitatio  spastica,  XII,  679,  690 
Nocturnal  epilepsy,  XI,  575;  XVI,  1058 
Noguchi's  test,  I,  74;  VIII,  419 
Nuclei,  cranial,  Lesions  of  the,  X,  493 

motor.    Symptoms    of    lesions    of 
the,  X,  493;  XXII,  1304 
facial,  XXII,   1331 
sixth,  XXII,  1327 
third,  XXII,  1323,  1326 
sensory,    Symptoms  of    lesions   of 
the,  XXII,  1302 
spinal  motor,  Symptoms  of  lesions  of, 
the,  XXII,  1304 
sensory,   Symptoms  of   lesions  of, 
XXII,  1302 
Nucleus  caudatus  and  lenticularis,  Localiz- 
ation in :    See  localization 
Numbness,  VI,  375;  XIV,  841 
Nyctalopia,  VI,  361 

Nystagmus,  I,  24;  IV,  291;  XXI,  1271-2 
Cerebellar,  I,  80 
Diseases  causing,  XII,  640 
Miner's,  XII,  684 
Myoclonic,   XII,   691 
Tests  for,  I,  30 

Observation,   Delusion  of,   XVI,   1113 

Tests  for  power  of,  I,  5 
Obstetrical  hand,  XI,  614 

paralysis,  IX,  454 
Obturator  neuralgia,  XV,  998 

paralysis,  XII,  718 
Occipital  headache,  XV,  948,  952 

lobe,  Symptoms  of  lesions  of  the,  XIV, 
850,  855;   XXI,   1285;   XXII,   1364-7 
neuralgia  or  neuritis,  XV,  948 
Occupation   in   nervous   diseases,   I,  2;   II, 
90 
neuroses,  II,  143;  XI,  616 
Ocular  ataxia,  XII,  649 

muscles,   Insufficiency  of  the,  XII,  692 
Locationof  paralysisof  the,  XXII, 

1316 
Paralysis  of  the,   XII,  700;   XIV, 

816 
Spasm  of  the,  XI,  590;  XIV,  816, 
876 
vertigo,  XII,  f>40 ;   XV,   1020 
Oesophageal  spasm,  XI,  617 


Olfaction.     Cortical  center  of,  p.  8 
Olfactory  sensation,  p.  7 
Onotogenetic  acts,  p.  23 
Ophthalmoplegia  completa,  X,  545 
externa,  X,  545;  XI,  590 
interna,  X,  545;  XI,  590 
progressiva,  X,  545 
sympathica,  XXI,  1268 
Ophthalmoscopic      examination,      Diseases 

revealed  by,   XIV,  819 
Ophthalmoscopy  in  examination  of  nervous 

patients,  I,  76 
Opisthotonus,  IV,  265;  XI,  590,  606 
Opium  poisoning;   XVI,   1054 

tremor,  XII,  673 
Oppenheim's  reflex,  I,  57;  V,  306 
Optic  aphasia,  III,  223;  XIII,  773 
atrophy,   XIV,  865 

Diseases  causing,  XIV,  898 
Senile,  XIV,  910 
chiasm,  p.  8 

Symptoms  of  lesions  of  the,  XIV, 
851,  860,  892;  XXII,  1319-20 
fasciculus  of  Gratiolet,  Lesion  of  the, 

XIV,  855-6;  XXII,  1364 
nerve.  Lesion  of  the,  XIV,  851,  862 
Perversion  of  vision  in  diseases  of 

the,  XIV,  844 
Symptoms    of    lesions    of,    XXII, 
1318 
neuritis,    Diseases   causing,    X,   507-8; 
XIV,  897 
followed   by  optic   atrophy,   XIV, 
909 
thalamus,  Symptoms  of  lesions  of  the, 
XII,  655;  XXI,  1275;  XXII,  1386 
Localization  in  the:     See  localiz- 
ation 
tract,   p.  8 

Symptoms  of  lesions  of  the.  XIV, 
858-9,  893;  XXII,  1321 
Orbit,    Symptoms    of    lesions    within    the, 

XIV,  914;  XXII,  1322 
Organic  diseases,   II,  136,  138 
hemiplegia,    XIII,   794 
reflex   acts,   I,   1 ;   V,  300,  3J3-4 ;    X. 
4;--;  XIV,  810 
Orthotonus,   IV,   265;   XI,  590,  606 
Oscedo,   XII,    731 
Osseous  sense,  Loss  of,  VI,  353 

Tests  for,  I,  56 
Osteitis  deformans,   XVII,   1182 
Osteo-arthropathy,    Hypertrophic    pulmon- 
ary, XVII,  1184 
Osteogenesis   imperfecta,   XVII,   1185 
Osteomalacia.  XVII,   1185 
Osteopsathyrosis.  XVII,   1185 
Ovarian  tenderness,  IX,  425 
Oxyakoia,  XIV.  B» 


277 


INDEX 


Pachymeningitis,   X,   502;   XI,   588;    XVI, 
1060 
Headache  in,  XV,  961 
hypertrophica  cervicalis,  X,  550 
interna  hemorrhagica,  X,  502;  XI,  588; 
XVI,   1060 
Paget's  disease,  XVII,  1182 
Pain,  pp.  6,  7,  11;  I,  1,  50;  VI,  374 
Diseases  causing,  XV,  931 
in  abdomen,  XV,  935 
back,   XV,   935 
extremities,  XV,  936 
head,  XV,  934 
nerve  distribution,  XV,  933 
thorax  and  abdomen,  XV,  935 
trunk,  XV,  935 
Girdle,  VI,  374 

Diseases  causing,  XV,  935 
Persistence  of,  I,  52 
Radiating,  VI,  374 

Retardation   of    conduction   of,   I,   51; 
VI,  381 
Palatine  arch,   High,  XVI,  1076 
Pallesthesia,  Tests  for,  I,  56 
Palsies,  Local,  IV,  259;  XII,  636 
Palpation     in     examination     of     nervous 

patients,    I,    c 
Pantophobia,  III,  235 
Paradoxical  pupillary  reflex,  V,  338 
reflex,  V,  318 
sensation,  VI,  379 
Parageusia,  VI,  391 
Paragraphia,  III,  226;  XIII,  777 
Parakinesis,  IV,  243 
Parakusis,  VI,  389;  XIV,  821 

Diseases  causing,  XIV,  821 
Paralysis,  I,  1,  21 ;  IV,  244 
Abducens,  XIV,  870 
Abductor,  laryngeal,  XIII,   756 
Acute  ascending,  II,  168;  X,  482 
agitans,  I,  20,  21;   XI,  612;  XII,  677; 

XIII,  766,  800 
Alcoholic,  X,  488 
Arsenical,  X,  488 
Atonic,  IV,  252;  X,  472 
Atrophic,   IV,   252;   X,  476-7.   547 

Acute:     See  poliomyelitis 
Chronic:       See     chronic    atrophic 
and  bulbar 
Axillary,  XII,  712 
Bell's  XII,  703 
Brachial    plexus,    IX,    454-5;    X,   490; 

XXII,  1306 
Brown-Sequard's,    IX,  442;     X,    509; 

XIV,  838 

Bulbar,   IX,  434;   X,    546;   XII,   694; 

xiii,  761 ;  xvii,  1150 

Cauda  equina,  X,  487;  XII,  721;  XV, 
1007;  XXII,  1308 


Paralysis,  Cervical  rib,  X,  556 

sympathetic,  XVII,  1191 
Choreic,  X,  510 
chronic,  Bone  atrophy   in,   XVII,  1 178 

Muscular   atrophy  in,   XVII,   1153 
continuous,  Diseases  causing,  X,  470 
Crico-arytenoid  XIII,  756 
Crico-thyroid,  XIII,  754 
Crossed,  IV,  256;  X,  537-42;  XV,  1017; 

XXI,  1268-70 

Crural,  XII,  717;  XV,  997 
of  diaphragm,  XII,  707 
Diphtheritic,  X,  488;  XIII,  753-4 
Diseases    causing,    IV,    244;    X,    469; 

XIV,  804;  XXII,  1290 
Diver's,  X,  521 
Erb's,  IX,  454;  X,  490 
External  rectus,  XIV,  870 
Facial,  XII,  703;  XIII,  751;  XIV,  928; 

XXII,  1317 

Family  periodic,  X,  555 
Flaccid,  IX,  252 

Diseases  causing,  X,  472 

Tests  for,  I,  33,  39 
Gluteal,  XII,  719 
Hypertonic,  IV,  251 ;  X,  473 
Hypoglossal,  XII,  706;  XIII,  752 
Hypotonic,  IV,  252;  X,  472 
Hysterical,  I,  21;  X,  527;  XIII,  747-8, 

759,   793;   XIV,   878;   XVI,   1074 
Infantile:     See  poliomyelitis  and  cere- 
bral palsy  of  childhood 
Inferior  oblique,    XIV,  875 

rectus,  XIV,  873 
Internal  rectus,  XIV,  871 
Intermittent,  X,  471 
Klumpke's,  IX,  455;  X,  490 
Labio-glosso-pharyngeal,  X,  546 
Landry's,  II,  168;   X,  482 
Laryngeal    nerve ;      Recurrent,     XIII, 
755 
superior,  XIII,  754 
Lead,  II,  158;  X,  494;  XIII,  788;  XVI, 

1050 
Levator  palati,  XIII,  753 
Local,  IV,  259;  XII,  636 
Localization  of  lesions  causing,  XXII, 

1290 
Median,  XII,  714 
Motor,  X,  469 

Diseases    causing,    XXII,     1295-6, 
1299,  1300 

Tests  for,  I,  33-4 
Motor  oculi,  XII,  700 
Musculo-cutaneous,  XII,  713 

-spiral,  XII,  716 
Myasthenic,    IV,    253 
Obstetric,  IX,  454 
Obturator,  XII,  718 
Phrenic,  XII,  707 


278 


INDEX 


Paralysis,  Pneumogastric,  XII,  704;  XIII, 
760 
Posticus  laryngeal,  XIII,  756 
Pseudo-bulbar,  X,  553 

Hypertrophic,  X,  500;  XVII,  1156 
Pterygoid,  XII,  702 
Radial,  XII,  716 
rectus,  External,  XIV,  870 
Inferior,  XIV,  873 
Internal,  XIV,  871 
Superior,  XIV,  874 
Recurrens,  XIII,  755 
Sciatic,  XII,  720 
sensory,  Diseases  causing,  XXII,  1294- 

6,   1298-1300 
Serratus,   XII,  709 
Spastic,  IV,  251 

Diseases  causing,  X,  473 
Spinal  accessory,  XII,  705 
Sub-scapular,   XII,   711 
Superior  laryngeal  nerve,  XIII,  754 
oblique,  XIV,  874 
rectus,  XIV,  872 
Supinator  longus,  XII,  716 
Supra-scapular,  XII,  708 
sympathetic   ganglia,   Diseases   causing 

XVII,  1142 
Tests  for,  I,  33-4 

Thoracic,  anterior  and  posterior,  XII, 
710 
Long,  XII,  709 
Thyreo-ary-epiglottis,  XIII,  754 
Tibialis,  XII,  720 

Trigeminus   (motor  branch),  XII,  702 
Trochlearis,  XV,  701 
Ulnar,  XII,  715 
Paralytic  dementia :     See  paresis 
and   flaccid  gait,  XIII,  741 

spastic    gait,    XIII,    742 
vaso-motor  reflex,  V,  326 
Paramyoclonus  multiplex,  XI,  603 
Paramyotonia  congenita,  IV,  265 ;  XI,  613 
Paranoia,  XVI,   11 13 
Paranoiacs,   p.    i<) 

Paranoid   form  of  insanity,  XVI,  1099 
Paraphasia,  III,  225;  XIII,  775 
Paraplegia,  I,  21;  IV,  257;  X,  480 

Ataxic,  X.  526;  XII,  660;  XIII,  796 
Disease  cutting,   X,  480 
dolorosa,  XV,  975 
Senile,  X.  522;   XIII,  791a 
Spastic,    X,   525;    Mil.   797 

II     134,   177;  XI,  570;  Ml. 

675;    XIII.    763;    MV.   895;    XVI, 

1 1.. i     XVIII,  iai6;  XIX,  1390 

Cerebri.  Ipiliaj  fluid  in,  VIII,  416,  419- 

20;  XIX,  1230 


Paresis,  Motor: 

Diseases  causing,  IV.  244;  X,  469 
Tests  for,  I,  34 
Optic  atrophy  in,  XIV,  912 
Paresthesiae,  p.  7 ;   I,  1  ;  VI,  375 
Parietal  lobes  and  lobule :     See  localization 
Parkinson's  disease:    See  paralysis  agitans 
Parosmia,  VI,  390 
Passive   contracture,   IV,   263 
Tremor,  IV,  289 

Diseases  causing.   XII,  646-7 
Pelvic  neuralgia,  XV,  952,  990 
Pemphigus,  XVII,  1168 
Perceptions,  p.  10 
Percussion     in     examination     of     nervous 

patients,  I,  c 
Perforating  ulcer,  XVII,  1172 
Periodic   family  paralysis,   X,   555 
Peripheral  neurons,  Disorders  of.   X.  472. 
474;   XIV,   804 
Location  of  lesions  of,  XXII,  1292 
motor  neurons,   IX,  462 

Diseases  of,  X,  472.  474 
sensory  neurons,  IX,  464 
Diseases  of,  XIV,  804 
Peroneal  paralysis,  XII,  720 
Peroneal  type  of  muscular  atrophy,  X.  496, 
Persecution,  Delusion  of,  XVI,  11 13 
Persistence  of  sensation,  VI,  382 

Tests  for,  I,  52 
Personal  factors  causing  nervous  diseases, 

II,  82 
Personality,  p.  16 

Double,  III,  209;  XVI.  1039 

Diseases  causing,  XVI,  1039 
Erroneous,  III,  208 
Pes  calcaneus  et  valgus.  XII.  720 
Pes  equino-varus,  XII,  720 
Petit  mal   (Le),  XI,  575;  XVI,   1058 
Pharyngeal  crises,  IX,  433 
Pharyngeal  reflex,  V,  315 

Tests  for,  I,  58 
Phobias,  III,  235;  XVI,  1072 
Photophobia,   VI,   371;   XII,  683 
Phrenic  neuralgia,  XV,  98s 
paralysis,  XII,  707 
spasm  or  cramp,  XII,  731 
Phylogcnctic  ads,   p.  23 
Physical  examination  of  patient.  I 
Physiological  introduction,  p.  5 
Pianist's  cramp.  XI,  616 
Picnic  acid  poisoning.  Xl\ 
Pill  rolling  movement  of  fingers,  XII,  677 
Pineal  gland      Diaeaac  of  tin-.  XXI    1270 
Pituitary   gland     Diseaaei    ■  if   the.    XXI. 
1279 
cunuchismu-.   \  \  I 
Plantar  reflex,  V,  303 

Tests  for.  I,  57 
Pleasure,  p.    1 1 


TO 


INDEX 


Pleurosthotonus,    IV,  265;   XI,   590,   606 
Plexuses,  brachial  and  lumbar,  Symptoms 
of  lesions  of,  IX,  454-5;  X,  490;  XXII, 
1306 
Pneumogastric   paralysis,   XII,   704;   XIII, 
-60 
spasm  or  cramp,  XII,  728 
Points  of  Valleix,  XV,  937,  942,  948,  977, 

989,  995-7 
Poisons,   I,   1;   II,  92,   164;  X,  482;   XIV, 

842 
Polioencephalitis  inferior,  Acute,  X,  544 
Chronic,  X,  546;  XII,  694;  XVII, 
1 150 
superior,  Acute,  X,  543;  XVI,  1064 
Chronic,  X,  545 
Poliomyelitis,  Acute  anterior,  II,  117,  167; 
X,    495;    XIII,    789;    XVII,    1 148; 
XIX,  1233 
Cerebro-spinal  fluid  in,  VIII,  416,  419; 
X,  495;  XIX,  1233 
Polyesthesia,   VI,  378 

Tests  for,  I,  54 
Polyneuritis,  II,  139,  160;  X,  488;  XII,  662; 
XIII,  787;  XIV,  823;  XV,  1008;  XVII, 
1147;  XXII,  1307 
Polyopia,  VI,  384 
Pons  Varolii,  Hemorrhage  or  softening  in, 

X,  539 

Localizing    symptoms    in :      See    local- 
ization 
Symptoms    of    lesions    of,    XIV,    883 ; 
XXII,  1328-31,  1353,  1383,  1388,  1398 
Tumor  of,  X,  540 
Ponto-cerebellar      angle,      Symptoms      of 

lesions  of,  IX,  438;  XXII,   1363 
Porencephalic  idiocy,  XVI,  1086 
Porencephaly,    II,    116;    X,   495,   501;    XI, 

577,  630;  XIII,  798;  XVI,  1048 
Position  sense,  Tests  for,  I,  41 
Post-epileptic     insanity,     XI,     575;     XVI, 
1058 ;    1 102 
coma,  XI,  575;  XVI,  1058 
febrile  insanity,  XXI,  1107a 
hemiplegic  ataxia,  XII,  655 
athetosis,  XI,  630-1 
chorea,  XI,  625 

contracture,  X,  504;   XI,  577,  619 
neuritic  contracture,  XI,  621 
paraplegic,  contracture,  X,  480,  548-51; 

XI,  620 

Posterior  column  or  horn :   See  spinal  cord, 
inferior  cerebellar  artery,  Thrombosis 
of,  XXI,  1268 
Postero-lateral  sclerosis,  X,  526;  XII,  660; 

XIII,  796 
Posticus  paralysis,  XIII,  756 
Pott's  disease,  I,  23;  II,  121;  X,  520 
Practice.    Effect  of,  p.  13 


Preputial  irritation,  IV,  251 
Pressure  sensation,  p.  6 
Pressure  sense,  Loss  of,  VI,  351 

Tests  for,  I,  49 
Priapism,  X,  512-5,  548-51;  XI,  607;  XIV, 

828 
Primary  dementia,  XVI,   1095 
Procursive  epilepsy,  IX,  575 
Prodromata  of  apoplexy,  IX,  432 

epilepsy,  IX,  430 
Progeria,  XVI,  1093 

Progressive  bulbar  paralysis,  X,  546;  XII, 
694;  XVII,   1 150 
muscular    atrophy:      See    amyotrophic 

lateral  sclerosis 
ophthalmoplegia:      See    polioencepha- 
litis superior  chronica 
Propulsion,  XI,  612 ;  XII,  677 ;  XIII,  766, 800 
Prosopalgia,  XV,  942 
Prosopoplegia,  XII,  703 
Protopathic  sensibility,   p.   6 
Pseudo-angina  pectoris,  XV,  984 
bulbar  paralysis,  X,  546,  553 
clonus,  IX,  425 

coma,  Diseases  causing,  XVI,  1038 
hypertrophic  paralysis,  I,  21;   X,  500; 

XVII,  1 156 
nystagmus,  XII,  640 
paresis,  XVI,  1101;  XVIII,  1208 
ptosis,  XVII,  1191;  XXI,  1268 
tabes :     See  neuritis,  multiple 
Psychasthenic  XV,  970;  XVI,  1072 
Psychic  blindness,   p.    10;    III,  232;   XXI, 
1285;  XXII,  1344 
localization  of,  XXI,  1285;  XXII, 
1344 
deafness,   p.    10;    III,   222,  233;    XIII, 

772;  XXI,  1284 
equivalent  of  epilepsy,  XI,  575 ;   XVI, 

1058 
trauma,  XVI,  1070 
Psychosis,  Korsakow's,  X,  488;  XVI,  1 100 
Ptarmus,  XII,  728 
Pterygoid  paralysis,  XII,  702 
Ptosis,  I,  24 

Pulmonary  osteo-arthropathy,   XVII,   1 184 
Pupillary  abnormalities,  I,  24;  XIV,  818 
diseases  causing,  XIV,  818 
opening,  Double,   XIV,  879 
reflex  acts,  V,  302 

Argyll-Robertson,  V,  332;  IX,  447; 

XIV,  891 
Accommodation,  V,  331 

Tests  for,  I,  27 
Consensual,  I,  25 ;  V,  330 
Direct,  I,  25 ;  V,  330 
Hemiopic,  I,  26;  V,  334;  XIV,  890 
Indirect,  I,  25;  V,  330 
Light,  I,  25;  V,  330 
Tests  for,  I,  25-7 


280 


INDEX 


Pupillary     reflex     acts,     Paradoxical,     V, 
338 

Pathology  of,  V,  302 

Physiology  of,  V,  302 

Westphal's,   V,  337 
Pupils,   Immobile,  V,  333;  X,  545 

Unequal,  V,  341 
Pulse  in  nervous  diseases,  I,  46 
Purulent  meningitis,  XI,  592;   XIX,  1227 

Cerebro-spinal  fluid  in,  XIX,  1227 

Quadrantic    hemianopia,    VI,    363 ;     XIV, 

815;  XXI,  1285;  XXII,  1343 
Quincke's  Disease,  XVII,  1201 
Quinine  vertigo,  XV,  1030 
Quinquand's  sign,  IX,  453 

Rabies,  II,  171;  XI,  607 
Race  in  nervous  diseases,  II,  88 
Radial  paralysis,  XII,  716 
Raptus  melancholicus,  XVI,  1112 
Raynaud's  disease,  XV,  1011;   XVII,  1195 
Reaction  of  completely  degenerated  muscle, 
VII,  404 
of   degeneration.   Electrical,   VII,  399, 
400 
Reading,    Diseases    causing    disorders    of, 
XIII,  735 
Tests  for,  I,  9 
Reasoning,  p.   14 
Recognition,  p.  11 
Rectal  crises,  IX,  433 

reflex,  V,  324 
Recurrens  paralysis,  XIII,  755 
Recurrent  insanity,  XVI,  1117 
Red    nucleus,    Symptoms    of    lesions    of, 
IX,  441;  XXI,   1270;   XXII,   1325 
vision,  XIV,  843 
Referred   pains,  VI,  374;   XV,  952 
Reflex,  Achilles,  I,  62;  V,  317 
acts,  p.  21 ;  V.  296 

abolition  of,  Diseases  causing,  X, 
472;  XIV,  810;  XXI,  1292 
Localization  of  diseases  caus- 
ing, XXII,  1292 
exaggeration  of,  Diseases  causing, 
X,    472;    XIV,    810;    XXI, 
1293 
localization  of  lesions  causing, 
XXII,  1293 
Inhibition  of,  V,  296-7 
Reinforcement  of,  I,  68 
Anal,  V,  307a 
Ankle,  I,  60;  V,  316-7 
arc,  p.  21 ;  V,  296 
Argyll-Robertson,  V,  332 

Physiology   and   pathology   of,   V, 
332 
Association,  p    .•_• 


Reflex,  Babinski's,  V,  304 

Tests  for,  I,  57 
Bechterew,  I,  63;  V,  320 
Bladder,  V,  323 
Cilio-spinal,  V,  335 
Conjunctival,  I,  58;  V,  312 
Corneal,  I,  58;  V,  312 
Cremasteric,  I,  57;  V,  308 
Cutaneous,  V,  297 

Tests  for,  I,  57 
Deep,  I,  60-6;  V,  299 
Dorsal  foot,  I,  63;  V,  320 
Elbow,  I,  64;  V,  321 
Epigastric,   I,  57;  V,  310 
Gluteal,  V,  307 

Tests   for,   I,   57 
Gordon's,  V,  305 
Hemiopic,  V,  334 

Tests  for,  I,  26 
Hyperemic,  V,  326 
Interscapular,  I,  57;  V,  311 
Ischemic,  V,  325 
Jaw,  I,  65;  V,  322 
Kernig's,  I,  66;  V,  319 
Knee,  I,  61 ;  V,  318 
Maxillary,  I,  65 ;  V,  322 
Mendel-Bechterew,  I,  63;  V,  320 
Mucous  membrane,  V,  298 

Tests  for,  I,  58 
Nasal,  I,  58;  V,  313 
Oppenheim's,  I,  57;  V,  306 
Organic,   I,   1 ;  V,  300,  323-4;  X,  472; 

XIV,  810 
Paradoxical,    V,  318,   338 
Pharyngeal,  I,  58;  V,  315 
Plantar,  V,  303 

Tests  for,  I,  57 
Pupillary,  V,  302 

to  accommodation,  V,  331 
Tests  for,  I,  27 

to  light,  V,  330 
Tests  for,  I,  25 
Rectal,  V,  324 

spasm,  IV,  268;  XI,  617;  XII,  637 
Superficial,  I,  57;  V,  297 
Tendon,  V,  299;  X,  472-3;  XIV,  810 

Tests    for,   I,   60-6 
Umbilical,  I,  57;  V,  309 
Uvular,  I,  58;  V,  314 
Vaso-motor,  V,  301 

Tests   for,   I,  59 
Vesical,  V,  323 
Westphal's  pupillary,  V,  337 
Wrist,  I,  64;  V,  321 
Riil,    Island  of,   Symptoms  of   lesions  of, 

XXI,  1278 
Reinforcement  of  reflexes,  I,  68 
Renal  crises,   IX.  4,(3 
Respiration,  Tests   for.  I,  45 


281 


INDEX 


Retardation    of    conduction    of    pain,    VI, 
38i 
Tests  for,  I,  51 
Retching,  V,  315 
Retina,  Perversion  of  vision  in  diseases  of, 

XIV,   844 
Retroactive  amnesia,  XIII,  769;  XVI,  1100 
Retrograde  amnesia,  XIII,  769 
Retropulsion,    XI,    612;    XII,    677;    XIII, 

766,  800 
Reverie,  p.   14 

Rheumatism  of  scalp,  XV,  962 
Rhythmical  chorea,  XI,  628 
Rigidity,  I,  31;  IV,  266;  XI,  590,  606,  612, 

614;  XII,  677;  XIII,  766,  800 
Rigors,  XII,  680 
Rinne's  test,  I,  15 
Risus  sardonicus,  XI,  606 
Romberg's  symptom,  I,  41 ;  IX,  448 
Rosenbach's  sign,  XVI,  1060-3 
Rotatory  epilepsy,  XI,  575 
Rubro-spinal   tract,    Symptoms    of    lesions 

of,  IX,  441;  XII,  676;  XXII,   1325 

Salaam  cramp,  XII,  690 

Saltatory  spasm,  XI,  618 

Sanity,  Tests  for,  I,  4 

Santonin  poisoning,  or  jaundice,  XIV,  842 

Saturnine :    See  lead 

Scalp,  Localized  edema  of,  XVI,  1044 

Rheumatism  of,  XV,  962 
Scapulo-humeral  type  of  muscular  atrophy, 

X,  499;  XVII,   1 151 
Schuller's  side  gait,  XIII,  793 
Sciatic  plexus,   Spasm   or  cramp  of,   XII, 

733 
Sciatica,  XII,  720;   XV,  996 
Scissors  gait,  X,  501 ;   XIII,  795-9 
Schmidt's  syndrome,   XII,  706 
Sclerodactylia,  VII,  1165 
Scleroderma,  I,  20;  XVII,  1165 
Sclerosis,    Amyotrophic    lateral,    X,    547 ; 
XII,  695;  XIII,  797;  XVII,  1149 
Combined  or   postero-lateral,   X,   526; 

XII,  660;  XIII,  796 
Disseminated  or  Multiple,  II,   149;  X, 

511;  XI,  580;  XII,  659,  668,  688; 
XIII,  756,  76s,  799;  XIV,  913; 

XIII,  796 

Optic  atrophy  in,  XIV,  913 
Vertigo  in,  XV,   1015 
Lateral,  X,  525;  XIII,  797 

Syphilitic,  of  Erb,  X,  525 
Postero-lateral,    X,    526;    XII,    660; 
XIII,   761 
Scoliosis,  I,  23 
Scotoma,  Glittering,  XIV,  846 

Homonymous,  XIV,  863 
Scurvy,  X,  495 


Seamstress'    cramp,   XI,   616 
Secondary  dementia,  XVI,  1 103 

deviation  of  sound  eye,  XIV,  816 
Tests  for,  I,  29 
Secretory     disorders,     Diseases      causing, 

XVII,  1145 
Semeiological  charts.     Introduction  to,  p.  5 
Semi-coma,  III,  206 

Diseases  causing,  XVI,  1037 
Senile  chorea,  XI,  624 

dementia,  p.  19;  XVI,  1105 
optic  atrophy,  XIV,  910 
paraplegia,  X,  522;  XIII,  791a 
tremor,    XII,   678 
Senility,  Fragility  of  bones  in,  XVII,  1185 
Sensation,  p.  9 
Auditory,  p.  8 
Conduction  of,  p.  6  et  seq. 
Cutaneous,  p.  6 

Difficulties   in   testing   for,    I,   47 
Diminution  of,  I,  47 ;   VI,  345 ;    XIV, 
80s 
Diseases  causing,  XIV,  805;  XXII, 
1 294- 1 300 
Disorders  of,  VI,  344;  XIV,  804 
Dissociation  of,  VI,  365;  XIV,  811 

Diseases  causing,  XIV,  811 
Double,  I,  54;  VI,  378 
Exaggeration  of,  VI,  346;  XIV,  806 

Diseases  causing,  XIV,  806 
General,    p.    8 
Gustatory,  p.  7 
Internal,  pp.  8,  10 
Light,  p.  8 

Localization  of,   I,  53;  XXII,   1290 
Muscle-joint,  p.  6 
Olfactory,  p.  7 
Painful,  p.  6 
Paradoxical,  VI,  379 
Persistence  of,  I,  52;  VI,  382 
Perversion  of,  VI,  347 

Diseases  causing,  XIV,  814;   XV, 
930 
Pressure,  p.  6;   I,  49 
Summation  of,  p.  9 
Tactile,  p.   6 
Temperature,  p.  6;  I,  55 
Tests  for,  I,  48 
Sensibility.     Deep,  p.  6 
Epicritic,   p.    6 
Head's  researches  on,  p.  6 
Protopathic,  p.  6 
Sensory  aphasia,  pp.  10,  28;  III,  222;  XIII, 
772;  XXII,   1345,  1368 
localization  of,  XXI,  1284;  XXII, 
134S,   1368 
Septic  insanity,  XVI,  1107a 
Serous  meningitis,  XI,  594;  XIX,  1239 

cerebro-spinal  fluid  in,  XIX,   1239 
Serratus  paralysis,  XII,   709 


282 


INDEX 


Sex  in  nervous  diseases,  II,  87 

Shaking  palsy:     See  paralysis  agitans 

Shivering,   XII,  680 

Shock,  I,  1 

Shoemakers'  cramp,  XI,  616 

Side  gait,  Schiiller's,  XIII,  793 

Sight,  p.  8 

Cortical  center  of,  p.  8 
Loss  of,  VI,  357 
Tests  for,  I,   12 
Simple  delusional  insanity,  XVI,  mo 
Simple   idiopathic   muscular  dystrophy,   X, 

498 
Singer's  cramp,  XI,  616 
Singultus,   XII,   731 

Sinus  thrombosis,  II,  182;  XV,  964;  XVI, 
1044 
headache  in,  XV,  964 
Sixth  cranial  nerve  or  nucleus 

Symptoms  of  lesions  of,  XXII,  1327-8 
Skill,  Loss  of.  III.  230;  IV,  249,  282 
Skin,  atrophy  of,  Diseases  causing,  XVII, 
1132 
eruptions,     Diseases     causing,     XVII, 

"34 
Glossy,  XVII,  1 160 
hypertrophy     of,      Diseases     causing, 

XVII,   1 133 
Trophic  lesions  of,  XVII,  1123 
ulcerations  of,  Diseases  causing,  XVII, 
"35 
Skull  in  disease,  I,  22;  XVII,  1181:     See 

also  cranium 
Sleep,  I,  18 

Sleeping  sickness,  II,  141 
Smell,  p.  7 

Diseases  causing  disorders  of,  XIV,  809 
Loss  of,  VI,  356 
Tests  for,  I,  16 
Sneezing,   V,   313;    XII,    728 
Snow  blindness,  VI,  360;   XIV,  843 
Softening,   Brain   stem,   X,   535;    XII,   656 
Cerebral.   X,  505-6;   XIV,   832;    XVI, 
1062-3 
in   crus  cerebri.    X,   537 
or  hemorrhage  in   brain   stem.    X. 

535 
in  medulla,   X,  541 
in  pons,  X,  539 
Somnambulistic  state.   Ill,  jno,  210 
Somnolence,  III,  207 
Sopor,   III,  207 
Soul      l  in-,  p,   17 
blindncn,  p    10 
deafm   i,  p    i" 
Spasm,  p.  j?  ;   I.  1 ;  XI    570 

abdonnn.il,    XII.  732 
in  asthma.    XI.  t,\- 

athetoldi   1 '■  tag,   XI.  57.1 

•     doneer**,  Ml.  736 


Spasm,  Blepharospasm,  XI,  601,  617:  XII, 

682.  726 
Brachial,  XII,   733 

choreiform.  Diseases  causing,  XI,  573 
Clonic,  IV.  246;  XI,  571 

Diseases  causing,  XI,  571 
Cornet  player's,  XII,  726 
or  cramp,  XI,  570 
Diseases  causing,  XI,  570 
Facial,  XII,  726 
Glosso-pharyngeal,  XII,  727 
Habit,  IV,  274;  XI,  626 
Hypoglossal,  XII,  729 
Hysterical,  XI,  618 
Intercostal,  XII,  732 
Irregular,  IV,  247 
in   Jacksonian   epilepsy,    IX,   431 ;    XI, 

587,  605 
Laryngismus   stridulus,    XI,  617:    XII, 

728 
Local,  XII   637 
Lumbar,  XII,  733 
Mobile,  IV,  271 
Occupation,  XI,  616 
Ocular  muscle,  XIV,  876 
Oesophageal,  XI,  617 
Phrenic,  XII,  731 
Pianist's,  XI,  616 
Pneumogastric,  XII,  728 
Reflex,   IV,  268;   XI,  617;   XII.  637; 

XVII.   iiy4 
Salaam  cramp  or,  XII,  690 
Saltatory,  XI,  618 
Sciatic,  XII,  733 
Seamstress',  XI,  616 
Shoemakers',  XI,  616 
Spinal  accessory,  XII,  730 
Telegraphers',  XI,  616 
Tests  for,  I,  32 
Tic  convulsive,  XI,  601 
douloureux,  XI,  602 
Tonic,  IV,  245;  XI,  57a 

Diseases  causing.  XI.  57 j 
Torticollis.  XII,  730 
Trigeminal,  XII,  725 
Typewriters',  XI,  616 
Urethral,  XI,  617 
Vesical,  XI,  617 
Violinists',   XI,  616 
Whooping  cough,   XI.  617 
Writers',  XI,  616 
Spasmus  glottidis,  XI.  oi;-;  XII.  ;vS 
mobilis,  IV,  .71 
ni. in. ins.   XII.   736 
nutans.  XI  I.  (71).  690 
Spastic  hemicrania,  XV.    111 
par.ih  -■  .    I  • 

for,  I.  .1.1.  .v) 
paraplegia,  X.  5.7;  XIII.  7.17 


283 


INDEX 


Special  senses,  Disturbances  of,  I,  I 
Special   symptoms  and  syndromes,  IX 
Speech,  p.  27 

Disorders  of,   XIII,  735 

Diseases  causing,  XIII,  735 
Tests  for  defects*  in,  I,  8 
Sphygmomanometer,  I,  46 
Spina  bifida  and  occulta,  I,  23;  II,  102;  X, 

523 
Spinal  abscess,  II,  152,  181 

accessory  paralysis,  XII,  705 
spasm  or  cramp,  XII,  730 
caries,  II,  121 

column  in  disease :     See  vertebral 
cord,   Endarteritis   and   thrombosis   of 
the,  XVIII,   1211 
Hemorrhage,    softening  or   injury 

of,  II,  146 
localization :     See  localization 
Symptoms    of     lesions    in,     above 
lumbar    enlargement,    XIII, 
795 
anterior     commissure,     XXII, 
1357,    1359 
horn,  XXII,  1304 
nerve  roots,  XXII,  1304 
Burdach's  column,  XXII,  1302 
cauda    equina,    X,    487;    XV, 

1007;    XXII,    1308 
cervical  enlargement,  X,  548-9, 
551;  XIV,  835-6;  XXII, 
1310 
region,    X,    512-5;    XIV, 
828;  XX,  1397 
conus  terminalis,  XIV,  830a 
dorsal  region,  X,  516-9;  XIV, 

829;   XXII,   1395 
lateral     column,      XII,     654; 
XVIII,    1212;    XXII,    1356, 
1358,  1360,   1396 
lumbar  enlargement,  X,  484-6; 
XIII,     791;      XIV,     825-6; 
XXII,  1309 
posterior   column,    XII,    654a; 
XIII,   785;    XXII,   1347. 
1350-1,  1396 
horn,  XXII,  1302 
nerve  roots,  XXII,  1302 
epilepsy,  I,  60-1;  IX,  443;  X,  509,  520; 

XIV,  838 
gumma,  XVIII,  1210 
hemiplegia,    IX,    442;    X,    509;    XIV, 

840;  XV,  981 
meninges,  Hemorrhage  in  the, 
meningitis,    Acute    and    chronic,    XI, 
608;   XV,  974,    1005;   XVIII,   1213-4 
muscular    atrophy,    Peroneal    type    of, 
X,  496;  XII,  696 
progressive,  X,  547 
nerves :    See  nerves 


Spinal  neuralgia,  XV,  971 

or  neuritic  muscular  atrophy,  X,  496; 

XII.  6o6 
nuclei :     See  nuclei 
segment.  Lesions  of.  XIV,  824 

Localization   in :     See   localization 
syphilis,    XVIII,    1210-6 
tenderness,  IX,  425 
tumor,  II,   151 ;   X,  486,  509,  515,  519, 
5+2,   55i;   XIV,  826,  836,   838;   XV, 
975.  981,   1006 
Spondylitis  deformans,  XV,  976 
Squint:     See   diplopia 
Stammering,  XII,  729;  XIII,  767-8 
Static  ataxia,  IV,  281;  IX,  448;  XII,  642 
Status  epilepticus,  XVI,  1058 
Stellwag's  sign,  XVII,   1 192-3 
Sternutatio  spastica,  XII,  728 
Stereognosis,  Tests  for,  I,  11 
Stereotypy,  XVI,  1096-8 
Stocking  form  of  anesthesia,  VI,  345 ;  IX, 

425 
Stokes-Adams  disease,  XI,  582;  XVI,  1057 

phenomenon,  IX,  436 
Strabismus  convergens,  XIV,  870 
deorsum  vergens,   XIV,  872,  875 
divergens,  XIV,  871 
sursum  vergens,  XIV,  873-4 
Strumpel's  tibialis  phenomenon,  IX,  445 
Strychnine  poisoning,  V,  297;  VI,  366;  XI, 

615 
Stupor,  III,  206;  XVI,  1095 
Stuttering,  XII,  729;  XIII,  767-8 
Subscapular  paralysis,  XII,  711 
Suggestion,    Susceptibility   to,   in    hysteria, 

IX,  425 
Suicide  in  nervous  diseases,  I,  2 
Sulfonal  poisoning,  X,  482 
Sunstroke   or   heatstroke,    XI,    589;    XVI, 
1068 
Headache  in,  XV,  966 
Superficial  reflex  acts,  I,  57;  V,  297 
Superior  laryngeal  paralysis,  XIII,  754 
oblique  muscle,  Paralysis  of,  XIV,  874 
rectus,  Paralysis  of,  XIV,  872 
Supra-orbital   neuralgia   or    neuritis,    XV, 

943 
Supra-scapular  paralysis,  XII,  708 
Surface  thermometers,  I,  78 
Sweating,   Excessive,   XVII,   1203 
Sydenham's  chorea,  XI,  622 
Symmetrical   gangrene,   XV,    ion;    XVII, 

"95 
Sympathetic   ganglionic    system,    Irritation 
of  the,  XVII,  1 143,  1 192 
Diseases  of  the,  XVII,  1128,  1143 

causing    disorders    of    the,    XVII, 
1121 
Paralysis  of  the,  XVII,  1142,  1191 


284 


INDEX 


Symptom-complexes  and  special  symptoms, 

IX 
Symptomatic  neuralgia,  XV,  937,  952 
epilepsy, 

mania,   XVI,   im 
melancholia,  XVI,   11 12 
Syncope,  XVI,  1056 

Local,  XVII,  1 195 
Syndromes  and  special  symptoms,  IX 
Synergy,  I,  41 

Syphilis,    I,    2:      See    also    cerebro-spinal 
syphilis 
Argyll-Robertson  phenomenon  in,  XIV, 

891 
Cerebro-spinal,  XVIII,  1214 
of  nervous  system,  XVIII,  1205 

Cerebro-spinal    fluid   in,   VIII,   410; 
XIX,  1232 
Optic  neuritis  in,  XIV,  903 
Vertigo  from,  XV,  1025,  1032 
Syphilitic  endarteritis  and  thrombosis,   II, 
175;  XVIII,  1207 
Cerebral,  XVIII,  1207 
Spinal,  XVIII,  1211 
lateral  sclerosis,  XVIII,  1212 
meningitis,  II,  173;  XV,  980a;  XVIII, 
1208-9 
Cerebral,  of  base,  XVIII,  1209 
of  convexity,  XVIII,  1208 
Cerebro-spinal,  XVIII,  1214 
Spinal,    XVIII,    1213 
nervous  diseases,  II,  94,  108;   XVIII, 

1205 
neuralgia,  XV,  951 
neuritis,   II,    174;   XVIII,   1215 
Syphilophobia,    III,   235 
Syringomyelia,    X,    552;    XII,    693;    XIII, 
798;  XIV,  837-9;  XV,  1009;  XVII,  1150a, 
1 170,  1 187;  XXII,  1357,  1359 

Tabes    dorsalis,    II,    133,    176;    XII,   661; 

XIII.  756,  784;  XIV,  827,  867,  894; 
XV,  979,  987.  1004;  XVIII,  1217; 
XIX.  1331 

Argyll-Robertson       phenomenon       in, 

XIV,  891 
Arthropathy  in,  XVII,  1186 
Cerebro-spinal  fluid  in,  VIII,  416,  419- 

20;   XIX,   1231 

Optic  atrophy  in,  XIV,  oil 

Perforating  ulcer  in,  XVII,  1172 

Vertigo  in,  XV,  1015 
Tabetic  crises.   IX,  4.13;  XV,  087 

cuirass,  VI,  345 
Tachycardia,  XII,  704,  XVII,   1193 
Tachcs  cerebrates,  V,  326;  XI,  590 
Tactile  sensations,  p.  6 

Talalgia,  XV,  1002 
Tapir  month,   X.  .107 


Taste,  p.  7 

Diseases    causing    disorders    of,    XIV, 

809 
Tests  for,  I,  17 
Teeth  as  cause  of  headache,  XV,  952 
Telegraphers'   cramp*  XI,   616 
Temperature  sense,  p.  6 
Loss  of,  VI,  350,  368 
Tests  for,  I,  55 
Temporal     convolution,     Lesions    of    the 
superior  lobe,  XXII,  1368 
Lesions  of,  causing  deafness,  XIV, 

923 
Localization   in :     See   localization 
Sensory  aphasia  in,  XXII,  1368 
Tendon  reflex  acts,  V,  299 

exaggerated,  Diseases  causing,  X, 

473;  XIV,  810 
diminished,    Diseases    causing,    X, 

472,  XIV,  810 
Tests  for,  I,  60-6 
Tenesmus,  XI,  617 
Terminal  dementia,  XVI,  1103 
Tetanus,  II,  170;  XI,  606 
neonatorum,  XI,  606 
Tetany,  II,  120;  XI,  614 
Tetartanopia,   VI,   363;    XIV,   815;    XXI, 

1285;  XXII,  1343 
Thermic  anesthesia,  VI,  350;  XIV,  810 
hyperalgesia,  VI,  367 
hyperesthesia.  VI,  366 
hypesthesia,  VI,  350 
Thermometry   in   examination   of   nervous 

patients,  I,  78 
Third  cranial  nucleus:     See  localization. 

nerve    or    nucleus,    Symptoms    of 
lesions  of,  XXII,    1323,   1326 
Thomsen's  disease,  II,  106;   IV,  265;  XI, 

613 
Muscular    hypertrophy    in,    XVII, 

"55 
Thoracic  paralysis,  XII,  709-10 
Thought,  p.   14 

Thrombosis,  Cerebral,  X,  506;  XVI,  1063; 
XVI II,  1207 
Posterior    inferior     cerebellar     artery, 

XXI,   1268 
Sinus,    II.    183;    XV,   064;    XVI.    1044 
Spinal.   XVIII.    1211 

Tibialis  paralysis,  XII,  7^0 

Thymus   gland)   lesion  of.   IV,   853 
Thyreo-ary-epiglottia  paralysis,   XIII.   754 
Tic.  articnlative,  XIII.  768 

convulsive,  IV,  267.  270;  XI.  601,  617; 

xii.  ja6 

douloureux.    IV,    -•<  7.    XI.    60a;    XII, 
726;   XV,  017 
Tingling,   VI.  373 
Tinnitus  annum,  1.  15;  VI,  388 
Tobacco  vertigo,  XV,  1030 


INDEX 


Tonic  spasm,  IV,  245 

Diseases  causing,  XI,  572 
Tonicity,  muscular,  I,  39;  IV,  240 
Tonometer  I,  46 
Tooth-Charcot-Marie's    type    of    muscular 

atrophy,  X,  496;  XII.  696 
Topoanesthesia,  VI,  376 
Torticollis,  XI,  601,  617;  XII,  730 
Toxic  coma,  XVI,  1067 

convulsion,  XI,  595-6 

headache,  XV,  963 

insanity,   XVI,   1107a 

nervous  diseases,  II,  92 

tremor,  XII,  673 

vertigo,  XV,  1029 
Trance,  XVI,  1069 
Transverse  myelitis,  XV,  980 
Transmission,  nervous,  pp.  5,  6 
Traumatic   nervous   diseases,   I,    1 ;   II,  91, 

135 
hysteria,  XVI,   1075 
neuroses,  II,  156;  XI,  616;   XII,  674; 
XVI,  1075 
Vertigo  from,  XV,  1033 
Tremor,  pp.  26-7;   II,   162;   IV,  250;  XII, 
639;   XXI,   1269-71 
Alcoholic,  XII,  673 
Asthenic,  XII,  671 
Diseases  causing,  XII,  639 
Essential,  XII,  681 
Hysterical,  XII,  674 
Intention,  IV,  290;  XII,  645 

Diseases  causing,  XII,  645 
Mercurial,  II,  159;  XII,  673 
Neurasthenic,  XII,  671,  674 
Nicotine,  XII,  673 
Opium,  XII,  673 
Passive,  IV,  289;  XII,  646-7 

Diseases  causing,  XII,  646-7 
Senile,  XII,  678 
Tests  for,  I,  31 
Toxic,  XII,  673 
Trigeminal  or  trifacial   neuralgia  or  neu- 
ritis, XV,  942,  946 
paralysis,  XII,  702 
spasm   or   cramp,   XII,   725 
Trional  poisoning,  X,  482 
Trismus,   IV,  265;  XII,  725 
Trochlearis  paralysis,  XII,  701 
Trophic  influences,  p.  29 

lesions,  Diseases  causing,  XVII,   1120, 
1 127 
Tests  for,  I,  40 
Trophoedcma,   XVII,   1202 
Trousseau's  sign,  IX,  450;  XI,  614 
Trypanosomiasis,   XVI,   1052 
Tuberculosis  in  nervous  diseases,  I,  2 
Tuberculous  meningitis,   II,    118,   122,   188; 
XI,  593;  XIX,  1228-9 
Cerebro-spinal  fluid  in,  XIX,  1228-9 


Tumor,  II,  187 

of  brain  stem,  X,  536 

Cerebral,  II,  151;  X,  507,  536-42;   XI, 

578,    587;    XIV,    833,    849.    855, 

861,    892,   908;    XV,   960;    XVI, 

1047 

Cerebro-spinal  fluid  in,  VIII,  411, 

419;  XIV,  1236 
Coma  in,  XVI,  1047 
Perversion  of  vision  in,  XIV,  849 
Vertigo  in,  XV,  1032 
of  cervical  enlargement  of  spinal  cord, 

x,  551 ;  xiv,  836 

region  of  spinal  cord,  X,  515 
crus  cerebri,  X,  538 
dorsal  region  of  spinal  cord,  X,  519 
lumbar  enlargement  of  spinal  cord, 

X,  486;  XIV,  826 
medulla,  X,  542 
optic  chiasm,  XIV,  860-1 
spinal,  II,  151 ;  X,  509 ;  XIV,  826,  836, 
838;  XV,  975,  98l,  1006 
Typewriters'  cramp,  XI,  616 
Typhus    fever,     Cerebro-spinal    fluid    in, 
XIX,  1235 


Ulcer,  Perforating,  XVII,  1 172 
Ulcerations,    Diseases    causing    cutaneous, 

XVII,  113S 
Ulnar  paralysis,  XII,  715 
Umbilical  reflex,  V,  309 

Tests  for,  I,  57 
Unconsciousness,  Tests  for,  I,  3 
Understanding,  Tests  for  defects  in,  I,  6 
Unequal  pupils,  V,  341 
Unverricht's  family  myoclonus  epilepticus, 

XI,  604 
Uremia,  II,  189 

Cerebro-spinal  fluid  in,   XIX,   1241 
Uremic  amaurosis,  XIV,  850 

coma,  XVI,  1066 

convulsion,  XI,  576,  581 

headache,   XV,  956 
Urethral  crises,  IX,  433 
Urethral  spasmodic  stricture,  XI,  617 
Urophobia,  III,  235 
Urticaria,  XVII,   1167 

Angio-neurotic,  XVII,  1201 

scripta,  XV,   1167 
Uvular   reflex,  V,  314 

Tests  for,  I,  58 

Vagus  paralysis,   XII,  704;   XIII,  760 

spasm,  XII,  728 
Valleix,  Points  of,  XV,  937.  942,  948,  977, 

989,  995-7 
Vascular      disorders.      Diseases      causing, 

XVII,  1 144 


286 


INDEX 


Vaso-motor    disorders.    Diseases    causing, 
XVII,  1129 

reflex  acts,  V,  301 

reflexes,  Tests  for,  I,  59 
Venery  in  nervous  diseases,  I,  2 
Vertebral  column  in  disease,  I,  23 
Vertex  headache,   XV,  952 
Vertige  paralysant,  XV,  1031 
Vertigo,   I,  1;   VI,  392;  XV,  932 

Alcoholic,  XV,  1030 

Apoplectic,  XV,  1026 

Atheromatous,  XV,  1025 

Aural,  XII.  650,  685;  XIV,  918;  XV, 
1019 

in  brain  stem  lesions,  XV,  1017 

Cardiac,  XV,  1024 

in  cerebellar  diseases,  XV,  1016 

in  cerebral  anemia,  XV,  1021,  1023 

Coffee,  XV,  1030 

Diseases  causing,  XV,  932 

Drug,  XV,   1030 

Epileptic,  XV,  1027 

Exhaustion,  XV,  1022 

in    fourth   ventricle   lesions,   XV,    1018 

Gerlier's  disease,  XV,  1031 

Hysterical,  XV,  1033 

Labyrinthine,  XII,  650,  685;  XIV,  918; 
XV,  1019 

Laryngeal,  IX,  433 

Meniere's,    XII,   650,   683;    XIV,   918; 
XV,  1019 

in  meningitis,  XV,   1032 

Migrainous,  XV,  1028 

Morphine,  XV,  1030 

Neurasthenic,  XV,   1033 

Nicotine,  XV,  1030 

Ocular,    XII,  649;    XV,   1020 

Paralysing,  XV,  1031 

Quinine,  XV,   1030 

Tabetic,   XV,    1015 

Tobacco,  XV,   1030 

Toxic,  XV,  1029 

in  traumatic  neuroses,  XV,    1033 
tumor,  XV,  103? 
sclerosis,   disseminated,    XV,    1015 

Syphilitic,  XV,  1025,  1032 
Vesical  crises,  IX,  433 

reflex,  V,  323 

spasm,  XI,  617 
Vibration   sense,   Loss  of,   VI,   353 

Tests  for,  I,  56 
Violinist's  cramp,  XI,  616 
Visceral  crises,    IX,  433 
Wlion,    Concentric   limitation   of   field   of, 
IX.  435;  XIV.  866;  XVI.  1074 

disturbances     of,     Diseases     causing, 
XIV.  807 


Vision,  Double,  XIV,  816 

Tests  for,  I,  12,  13.  14 

field  of,  Tests  for,  I,  14 

Green,  XIV,  844 

limitation  of  field  of,  Diseases  causing, 
XIV,  815 

localization  of,  Disturbances  of,  XXII, 
1315 

Loss  of,  XIV,  850-1 

Perversion  of,  XIV,  814 

Red,  XIV,  843 

Tests  for,  I,  12,  13,  14 

Yellow,  XIV,  842 
Visual  aphasia,  III,  223;  XIII,  773 

axis,  Displacement  of,  I,  28;  XIV,  816 
Vitiligo,  XVII,  1 162 
Vocal  cords,  Paralysis  of,  XIII,  753-60 
Voltoni's  disease,  XV,  1019 
Voluntary  motion,  p.  22 

Disorders  of,  IV,  240 
Vulvo- vaginal  crises,  IX,  433 

Walk,  Inability  to,  in  disease,  I,  21 
Wassermann  reaction,  VIII,  420 
Weakness,  XIII,  790 

Tremor  from,  XII,  671 
Weber's  law,  p.  9 

syndrome,   IX,  440;   XXI.   1270 

tests,  I,  15 
Wernicke's  polioencephalitis  superior 

hemorrhagica  acuta,   XVI,   1064 

scheme  of   aphasia,  XIII,   739 
Westphal-Edinger  nucleus,  V,  330 
Westphal's  pupillary  reflex,  V,  337 
Whooping   cough,   XI,   617 
Will,   p.   24 

Free,  pp.  23-4 

-power,  p.  24 
Word  blindness.   III,  228.  233;  XIII,  77J 

deafness,   III,  222;  XIII,  772 
Worry,    I.    1 

Wounds,  II.  145 

Wrist-drop.    X.    404;     XI.    584;    XII,    716 
reflex,  Y,  331 

Tests   for,    I.   64 
Writer's  cramp.   XI,  616 
Writing,    Diseases    causing    disorders    of, 
XIII.   735 
Tests  for  defects  in,   I,   10 
Wrv  neck,  XII.  ;.!<> 

Xanthopsia,   XIV, 

*i  awning,  XII,  731 
yellow  vision,  \i  V,  842 


47 


COLUMBIA   UNIVERSITY   LIBRARIES 

This  book  is  due  on  the  date  indicated  below,  or  at  the 
expiration  of  a  definite  period  after  the  date  of  borrowing,  as 
provided  by  the  library  rules  or  by  special  arrangement  with 
the  Librarian  in  charge. 

DATE  BORROWED 

DATE  DUE 

DATE  BORROWED 

DATE  DUE 

' 

C28I3-52) IOOM 

